count source_label source_id relationship target_label target_id entity_type solr_id publication_id sentences
10 COL5A1 UNIPROT:P20908 activates MESH:D063646 Phenotype 6af9f95e-1a78-11f0-b759-0050569a791b 10.1016/j.cellsig.2024.111419 Importantly, COL5A1 deletion effectively inhibited the tumorigenesis of cholesterol-resistant ovarian cancer cells.|||Therefore, the present results strongly suggested that both COL5A1 depletion and PARP1 inhibition significantly impeded the tumorigenesis of cholesterol-resistant ovarian cancer cells, concomitant with a decrease in EMT progression.|||Furthermore, COL5A1 depletion dramatically inhibited tumorigenesis in these cells, accompanied by reduced EMT progression.|||COL5A1 depletion inhibited the tumorigenesis of cholesterol-resistant ovarian cancer cells We next explored the functional consequences of COL5A1 in cholesterol-resistant ovarian cancer cells.|||Intriguingly, both COL5A1 depletion and PARP1 inhibition significantly impeded the tumorigenesis of these cells, concomitant with a decrease in EMT progression.
8 UNIPROT:Q6ZV60 decreases COL5A1 UNIPROT:P20908 Protein 784f571c-1b9e-11f0-bb75-0050569a1f61 10.1016/j.prp.2024.155238 In addition, LINC00173 inhibits OSCC cell angiogenesis by inhibiting COL5A1 transcription through targeting GATA6[148].
6 COL5A1 UNIPROT:P20908 activates MESH:D002784 Phenotype 6af9f95e-1a78-11f0-b759-0050569a791b 10.1016/j.cellsig.2024.111419 COL5A1 depletion inhibited the tumorigenesis of cholesterol-resistant ovarian cancer cells We next explored the functional consequences of COL5A1 in cholesterol-resistant ovarian cancer cells.|||Therefore, the present results strongly suggested that both COL5A1 depletion and PARP1 inhibition significantly impeded the tumorigenesis of cholesterol-resistant ovarian cancer cells, concomitant with a decrease in EMT progression.|||Importantly, COL5A1 deletion effectively inhibited the tumorigenesis of cholesterol-resistant ovarian cancer cells.
6 UNIPROT:Q05397 increases COL5A1 UNIPROT:P20908 Protein 6af9f95e-1a78-11f0-b759-0050569a791b 10.1016/j.cellsig.2024.111419 In summary, these data collectively revealed that activated FAK/Src signaling upregulated COL5A1 expression in cholesterol-resistant ovarian cancer cells.|||Here, we demonstrated that activated FAK signaling in cholesterol-resistant ovarian cancer cells induced COL5A1 expression.
4 COL5A1 UNIPROT:P20908 activates UNIPROT:P02774 Protein b2aaba70-0021-11f0-9c09-0050569a791b 10.1016/j.prp.2024.155778 Also, HOTAIR controls GC growth and metastasis by sponging miR-1277–5p and upregulating COL5A1, and COL5A1-mediated GC cell proliferation may be mediated by impacts on the TME, revealing new targets for GC therapy[61].
4 COL5A1 UNIPROT:P20908 activates GO:0008283 Phenotype 6af9f95e-1a78-11f0-b759-0050569a791b 10.1016/j.cellsig.2024.111419 As expected, COL5A1 knockdown significantly inhibited the proliferation and invasion of ID8-R, A2780-R and OVCAR3-R cells (Fig. 4B and C).
4 COL5A1 UNIPROT:P20908 activates MESH:D009361 Phenotype 6af9f95e-1a78-11f0-b759-0050569a791b 10.1016/j.cellsig.2024.111419 As expected, COL5A1 knockdown significantly inhibited the proliferation and invasion of ID8-R, A2780-R and OVCAR3-R cells (Fig. 4B and C).
4 COL5A1 UNIPROT:P20908 inhibits MESH:D010455 Phenotype d767df08-bc3f-11e5-8d2d-001a4ae51247 10.1016/j.matbio.2004.09.004 The anti-COL5A1 antibody (goat polyclonal IgG) and the COL5A1 blocking peptide were purchased from Santa Cruz Biotechnology.
4 COL5A1 UNIPROT:P20908 activates GO:0016477 Phenotype e1042f6a-3b32-11e9-8325-001a4a160175 PMC6369854 COL5A1 knockdown significantly inhibited cell proliferation, induced cell apoptosis, inhibited cell migration and invasion in vitro, and inhibited tumor growth in vivo.|||In addition, COL5A1 knockdown also significantly inhibited cell migration and invasion in vitro, suggesting that COL5A1 is involved in malignancy of ccRCC.|||COL5A1 knockdown using siRNA inhibited cell proliferation, induced cell apoptosis, inhibited cell migration and invasion in vitro, and inhibited tumor growth in vivo.|||COL5A1 knockdown inhibits ccRCC cell migration and invasion in vitro.
4 COL5A1 UNIPROT:P20908 activates GO:0008283 Phenotype e1042f6a-3b32-11e9-8325-001a4a160175 PMC6369854 COL5A1 knockdown inhibits ccRCC cell proliferation and induces apoptosis in vitro.|||COL5A1 knockdown using siRNA inhibited cell proliferation, induced cell apoptosis, inhibited cell migration and invasion in vitro, and inhibited tumor growth in vivo.|||We observed that a transient knockdown of COL5A1 significantly inhibited cell proliferation and induced cell apoptosis in vitro.|||COL5A1 knockdown significantly inhibited cell proliferation, induced cell apoptosis, inhibited cell migration and invasion in vitro, and inhibited tumor growth in vivo.
4 COL5A1 UNIPROT:P20908 activates MESH:D009369 Phenotype e1042f6a-3b32-11e9-8325-001a4a160175 PMC6369854 Overexpression of COL5A1 promotes tumor progression and metastasis and correlates with poor survival of patients with clear cell renal cell carcinoma.|||COL5A1 knockdown using siRNA inhibited cell proliferation, induced cell apoptosis, inhibited cell migration and invasion in vitro, and inhibited tumor growth in vivo.|||COL5A1 knockdown significantly inhibited cell proliferation, induced cell apoptosis, inhibited cell migration and invasion in vitro, and inhibited tumor growth in vivo.|||Moreover, deletion of COL5A1 expression significantly inhibited tumor growth in vivo using siRNA technique.
4 COL5A1 UNIPROT:P20908 activates MESH:D009361 Phenotype 23705ecc-ae95-11ec-ae7b-0050569a1f61 PMCPMC8079757 "Previous study by Feng G et al. has found COL5A1 promoted ccRCC cell proliferation, apoptosis, migration, invasion in vitro (32).|||The results showed that overexpression of COL5A1 could partially reverse the inhibition of cell proliferation and invasion by miR-582-5p.In addition, the upstream regulators such as transcription factors may be responsible for dysregulated expression of miRNAs in cancers.|||The functional relevance of COL5A1 targeting by miR-582-5P was investigated by determining whether COL5A1 overexpression could rescue the inhibitory effects of miR-582-5p on ccRCC cell proliferation and invasion.|||Transwell assays showed that the invasion ability inhibited by miR-582-5p was remarkably rescued by the COL5A1 overexpression (
Figure 5D
)."
4 COL5A1 UNIPROT:P20908 activates MESH:D009361 Phenotype e1042f6a-3b32-11e9-8325-001a4a160175 PMC6369854 COL5A1 knockdown significantly inhibited cell proliferation, induced cell apoptosis, inhibited cell migration and invasion in vitro, and inhibited tumor growth in vivo.|||COL5A1 knockdown inhibits ccRCC cell migration and invasion in vitro.|||In addition, COL5A1 knockdown also significantly inhibited cell migration and invasion in vitro, suggesting that COL5A1 is involved in malignancy of ccRCC.|||COL5A1 knockdown using siRNA inhibited cell proliferation, induced cell apoptosis, inhibited cell migration and invasion in vitro, and inhibited tumor growth in vivo.
4 UNIPROT:P49895 decreases COL5A1 UNIPROT:P20908 Protein edad6572-340a-11e8-bf76-001a4a160175 27940296 In KIJ265T cells devoid of ectopic DIO1 expression supplementation with rT3 decreased expressions of Cyclin E2, COL5A1, and ITGB3; however, these effects were much smaller than the changes introduced by DIO1 overexpression.
4 UNIPROT:P12931 increases COL5A1 UNIPROT:P20908 Protein 6af9f95e-1a78-11f0-b759-0050569a791b 10.1016/j.cellsig.2024.111419 In summary, these data collectively revealed that activated FAK/Src signaling upregulated COL5A1 expression in cholesterol-resistant ovarian cancer cells.
4 FPLX:TGFB increases COL5A1 UNIPROT:P20908 ProteinFamily d767df08-bc3f-11e5-8d2d-001a4ae51247 10.1016/j.matbio.2004.09.004 Our results indicate that TGF-β1 significantly up-regulates COL5A1 mRNA expression (3.2-fold increase in lanes 2 and 5) in MC3T3-E1 cells, thereby confirming the results of the cDNA microarray.
4 FPLX:TGFB activates COL5A1 UNIPROT:P20908 ProteinFamily d767df08-bc3f-11e5-8d2d-001a4ae51247 10.1016/j.matbio.2004.09.004 In the much more sensitive Northern analysis, induction of Collagen 1 (α1) was less relative to the TGF-β1 induction of COL5A1 (Fig. 1A).
4 UNIPROT:P09874 activates COL5A1 UNIPROT:P20908 Protein 6af9f95e-1a78-11f0-b759-0050569a791b 10.1016/j.cellsig.2024.111419 These findings collectively substantiate the notion that PARP1 induces COL5A1 upregulation through the activation of FAK/Src signaling in cholesterol-resistant ovarian cancer cells.
4 MESH:D002784 increases COL5A1 UNIPROT:P20908 Phenotype 6af9f95e-1a78-11f0-b759-0050569a791b 10.1016/j.cellsig.2024.111419 In this study, our findings revealed that long-lasting cholesterol exposure significantly promoted COL5A1, COL12A1 and COL3A1 expression in ovarian cancer cells (Fig. 3A).|||Here, we demonstrated that activated FAK signaling in cholesterol-resistant ovarian cancer cells induced COL5A1 expression.
3 COL5A1 UNIPROT:P20908 activates UNIPROT:P02774 Protein ec58cd60-f577-11eb-8f00-001a4a160176 32583079 In addition, COL5A1-mediated GC cell proliferation and metastasis were regulated by the HOTAIR/miR-1277-5p axis.|||In addition, overexpression of COL5A1-enhanced GC growth, possibly through facilitating immune infiltration, while miR-1277-5p mimics exerted the reverse effects on GC development.|||We further demonstrated that COL5A1 was highly expressed in GC cells and tissues, and knockdown of COL5A1 repressed the proliferation of GC cells, which was regulated by the HOTAIR/miR-1277-5p axis.
3 COL5A1 UNIPROT:P20908 activates GO:0008283 Phenotype 23705ecc-ae95-11ec-ae7b-0050569a1f61 PMCPMC8079757 "Previous study by Feng G et al. has found COL5A1 promoted ccRCC cell proliferation, apoptosis, migration, invasion in vitro (32).|||The functional relevance of COL5A1 targeting by miR-582-5P was investigated by determining whether COL5A1 overexpression could rescue the inhibitory effects of miR-582-5p on ccRCC cell proliferation and invasion.|||CCK-8 assay and colony formation assay suggested that the overexpression of COL5A1 rescued the inhibitory effect of miR-582-5p on cell proliferation in vitro (
Figures 5B, C
)."
3 COL5A1 UNIPROT:P20908 activates GO:0006915 Phenotype e1042f6a-3b32-11e9-8325-001a4a160175 PMC6369854 COL5A1 knockdown inhibits ccRCC cell proliferation and induces apoptosis in vitro.|||COL5A1 knockdown using siRNA inhibited cell proliferation, induced cell apoptosis, inhibited cell migration and invasion in vitro, and inhibited tumor growth in vivo.|||COL5A1 knockdown significantly inhibited cell proliferation, induced cell apoptosis, inhibited cell migration and invasion in vitro, and inhibited tumor growth in vivo.
2 COL5A1 UNIPROT:P20908 increases HGNC:33510 Protein ec58cd60-f577-11eb-8f00-001a4a160176 32583079 In the present study, we found that HOTAIR and COL5A1 were overexpressed in GC cell lines and that overexpression of HOTAIR promoted the proliferation and metastasis of GC by sponging miR-1277-5p and upregulating COL5A1.
2 COL5A1 UNIPROT:P20908 actelytatesProtein CHEBI:39010 Chemical 318e99b0-ae95-11ec-ae7b-0050569a1f61 PMCPMC8691835 Multiple regions around the Collagen Type V Alpha 1 Chain (COL5A1) gene, up to 100 kb upstream of the TSS, were found to be specifically acetylated in MES lines, and we included a total of seven into the library (Figure 3c.
2 COL5A1 UNIPROT:P20908 inhibits GO:0006412 Phenotype fedad284-97c5-11e8-b8fa-001a4a160176 PMC6070246 Within the network of post-translational modification, BDE-99 also up-regulated a series of genes involved in protein degradation such as serine protease, trypsinogen, and chymotrypsin, but down-regulated many collagen-related protein synthesis, such as collagen type V alpha 1 chain (Col5a1), Col3a1, ERBB receptor feedback inhibitor 1 (Errfl1),serpin family H member 1 (Serpinh1), and phospholipase C beta 3 (Plcb3).
2 COL5A1 UNIPROT:P20908 inhibits MESH:D003094 Phenotype fedad284-97c5-11e8-b8fa-001a4a160176 PMC6070246 Within the network of post-translational modification, BDE-99 also up-regulated a series of genes involved in protein degradation such as serine protease, trypsinogen, and chymotrypsin, but down-regulated many collagen-related protein synthesis, such as collagen type V alpha 1 chain (Col5a1), Col3a1, ERBB receptor feedback inhibitor 1 (Errfl1),serpin family H member 1 (Serpinh1), and phospholipase C beta 3 (Plcb3).
2 COL5A1 UNIPROT:P20908 activates GO:0001503 Phenotype d767df08-bc3f-11e5-8d2d-001a4ae51247 10.1016/j.matbio.2004.09.004 Further studies of COL5A1 and other genes identified through our cDNA microarray analysis will likely lead to the discovery of new markers for osteogenesis as well as new targets of TGF-β, shedding further light on TGF-β signaling and its role in osteogenesis.
2 COL5A1 UNIPROT:P20908 activates GO:0001837 Phenotype 6af9f95e-1a78-11f0-b759-0050569a791b 10.1016/j.cellsig.2024.111419 Conversely, FAK inhibitors effectively blocked COL5A1 expression, thereby inhibiting EMT progress.
2 COL5A1 UNIPROT:P20908 activates GO:0001837 Phenotype 1ce8f3ea-c68d-11ee-b346-0050569a791b 10.1016/j.pharmthera.2023.108576 Their study demonstrated that NAT10 can write ac4C modification in the 3′ UTR of COL5A1(Collagen type V Alpha 1 chain) mRNA, thereby enhancing the stability ofCOL5A1mRNA and promoting gastric cancer cell EMT(Epithelial-Mesenchymal transition) and metastasis (Zhang, Jing, Wang, et al., 2021a).
2 COL5A1 UNIPROT:P20908 activates FPLX:COL1 ProteinFamily 3ed19a0a-1be8-11f0-aa93-0050569a1f61 10.1016/j.tjog.2024.01.021 COL5A1 is involved in the formation of type V collagen, which is widely distributed in tissues and contributes to collagen fibrillogenesis in combination with type I collagen.
2 COL5A1 UNIPROT:P20908 activates UNIPROT:Q16769 Protein 743deed8-753a-11ee-add2-0050569a791b 10.1007/s10528-022-10307-3 **p< 0.01 compared to Het-1A.EThe correlation between COL5A1 and miR‐361‐3p was assessed using Pearson’s correlation analysis COL5A1 Promotes EC Development by Interacting with miR-361-3p To further examine cellular functions of the miR-361-3p/COL5A1 axis, COL5A1 and miR-361-3p were knocked down, and knockdown efficiency was examined at the protein level.|||Taken together, our findings suggested that the miR-361-3p downstream target, COL5A1, could enhance EC progression.Fig.
2 COL5A1 UNIPROT:P20908 activates GO:0008283 Phenotype ec58cd60-f577-11eb-8f00-001a4a160176 32583079 We further demonstrated that COL5A1 was highly expressed in GC cells and tissues, and knockdown of COL5A1 repressed the proliferation of GC cells, which was regulated by the HOTAIR/miR-1277-5p axis.|||Therefore, we speculated that COL5A1-mediated cell proliferation was partially achieved by an increase in immune cell infiltration, which may be regulated by the HOTAIR/miR-1277-5p axis.
2 COL5A1 UNIPROT:P20908 activates MESH:D009362 Phenotype d139baec-8285-11ee-ae93-0050569a1f61 10.1007/s00109-022-02264-6 Overexpression of COL3A1 leads to the metastasis of breast cancer, while overexpression of COL5A1 leads to the metastasis of lung adenocarcinoma [47–50].|||These data are worth considering to determine whether gastric cancer metastasis induced by COL5A1 or the lncRNA HOTAIR/miR-1277-5p/COL5A1 axis is achieved by increasing the level of immune cell infiltration [57–59].
2 COL5A1 UNIPROT:P20908 activates MESH:D009362 Phenotype e1042f6a-3b32-11e9-8325-001a4a160175 PMC6369854 Overexpression of COL5A1 promotes tumor progression and metastasis and correlates with poor survival of patients with clear cell renal cell carcinoma.|||Moreover, COL5A1 mRNA expression in patients with metastatic ccRCC was significantly higher than those with localized ccRCC, suggesting overexpression of COL5A1 could promote metastasis of ccRCC.
2 COL5A1 UNIPROT:P20908 inhibits GO:0006915 Phenotype e1042f6a-3b32-11e9-8325-001a4a160175 PMC6369854 Apoptosis analysis revealed that knockdown of COL5A1 significantly increased apoptosis of Caki-1 cells (Figure 3D).|||We observed that a transient knockdown of COL5A1 significantly inhibited cell proliferation and induced cell apoptosis in vitro.
2 COL5A1 UNIPROT:P20908 activates MESH:D010013 Phenotype 787f09a2-3c6a-11f0-afc2-0050569a791b 10.1016/j.prp.2022.154013 "
[77]
Z.
Lin
J.
Zeng
X.
Wang
Compound phenotype of osteogenesis imperfecta and Ehlers-Danlos syndrome caused by combined mutations in COL1A1 and COL5A1
Biosci.|||Rep.
39
2019
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Lin Z., Zeng J., Wang X. Compound phenotype of osteogenesis imperfecta and Ehlers-Danlos syndrome caused by combined mutations in COL1A1 and COL5A1."
2 COL5A1 UNIPROT:P20908 activates MESH:D004535 Phenotype 787f09a2-3c6a-11f0-afc2-0050569a791b 10.1016/j.prp.2022.154013 "Rep.
39
2019
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Lin Z., Zeng J., Wang X. Compound phenotype of osteogenesis imperfecta and Ehlers-Danlos syndrome caused by combined mutations in COL1A1 and COL5A1.|||
[77]
Z.
Lin
J.
Zeng
X.
Wang
Compound phenotype of osteogenesis imperfecta and Ehlers-Danlos syndrome caused by combined mutations in COL1A1 and COL5A1
Biosci."
2 PR:000000617 activates COL5A1 UNIPROT:P20908 Protein a6c2399a-ae94-11ec-840e-0050569a791b PMCPMC8766495 Our GSEA revealed a downregulation of ECM-related genes uponCEBPB-knockout in BT-20 cells, and LAP re-expression in BT-20CEBPB-ko cells results in upregulation of pro-metastatic factors FN1, TNC, THBS1, COL5A1 and MMP2.
2 MESH:D002784 activates COL5A1 UNIPROT:P20908 Phenotype 6af9f95e-1a78-11f0-b759-0050569a791b 10.1016/j.cellsig.2024.111419 Further study would be needed to explore the detail mechanisms concerning how high levels of cholesterol help p-FAK promoting an increase of COL5A1, and help PARP1 directly bind to FAK.
2 FPLX:TGFB activates COL5A1 UNIPROT:P20908 ProteinFamily 4c4cb736-3514-11e8-bf76-001a4a160175 26794903 In mouse flexor tendon tenocytes, TGF-β1 up-regulated Scx, Mkx, Bgn, Col5a1, Col12a1, and PAI-1 in a dose-dependent manner[30].
2 UNIPROT:P09874 increases COL5A1 UNIPROT:P20908 Protein 6af9f95e-1a78-11f0-b759-0050569a791b 10.1016/j.cellsig.2024.111419 Mechanistically, PARP1 upregulated COL5A1 levels through directly binding to FAK.
2 UNIPROT:Q01196 increases COL5A1 UNIPROT:P20908 Protein 23705ecc-ae95-11ec-ae7b-0050569a1f61 PMCPMC8079757 "Over-expression of RUNX1 led to decreased miR-582-5p expression and increased COL5A1 expression, which demonstrates that there is an axis among RUNX1/miR-582-5p/COL5A1 signaling.|||Overexpression of RUNX1 led to decreased miR-582-5p and increased COL5A1 expression which indicated that there was an axis among RUNX1/miR-582-5p/COL5A1 signaling (
Figures 6E, F
)."
1 COL5A1 UNIPROT:P20908 activates UNIPROT:A0A1D6EFT8 Protein e546d0b8-ae94-11ec-a61d-0050569a1f61 PMCPMC8470511 Their results suggest that a combination of COL5A1 and COL1A1 mutations may lead to compound phenotypes of OI and EDS, while COL1A1 (c.2010delT) may result in OI.On the other hand, there have not been any studies investigating the association between previously mentioned COL5A1 gene polymorphisms and TMJ internal derangements, including ADDwoR.
1 COL5A1 UNIPROT:P20908 inhibits UNIPROT:P02462 Protein a5f2ddce-c8b1-11ee-b346-0050569a791b PMC10017276 Protein processing in the endoplasmic reticulum (upregulated Dnajb11; downregulated Ckap4 and Man1a2), peroxisomes (upregulated Pex6, Pex11g, Hacl1, and Phyh; downregulated Acsl5 and Pmvk), mitochondrial oxidative respiratory chain (upregulated Ndufa4, Ndufaf1, and Xox4i2), membrane transporters (upregulated Cacng3, Atp1a4, and Slc8a2; downregulated Slc1a1), and extracellular matrix (upregulated Col5a1; downregulated Col4a1 and Col25a1) was dysregulated in the infected hippocampus; however, the alterations were mild (Fig. 6B).
1 COL5A1 UNIPROT:P20908 inhibits UNIPROT:Q9BXS0 Protein a5f2ddce-c8b1-11ee-b346-0050569a791b PMC10017276 Protein processing in the endoplasmic reticulum (upregulated Dnajb11; downregulated Ckap4 and Man1a2), peroxisomes (upregulated Pex6, Pex11g, Hacl1, and Phyh; downregulated Acsl5 and Pmvk), mitochondrial oxidative respiratory chain (upregulated Ndufa4, Ndufaf1, and Xox4i2), membrane transporters (upregulated Cacng3, Atp1a4, and Slc8a2; downregulated Slc1a1), and extracellular matrix (upregulated Col5a1; downregulated Col4a1 and Col25a1) was dysregulated in the infected hippocampus; however, the alterations were mild (Fig. 6B).
1 COL5A1 UNIPROT:P20908 activates UNIPROT:Q13315 Protein 0e9e3a84-5c1d-11e7-b441-001a4ae51247 PMC5396846 "CXCL10 may be of benefit in ATC treatment, FOS may be involved in ATC formation,
COL5A1 and COL11A1 may promote the progression of ATC, and IL8 may act as a biomarker
for the diagnosis of ATC."
1 COL5A1 UNIPROT:P20908 activates UNIPROT:P10184 Protein e546d0b8-ae94-11ec-a61d-0050569a1f61 PMCPMC8470511 Their results suggest that a combination of COL5A1 and COL1A1 mutations may lead to compound phenotypes of OI and EDS, while COL1A1 (c.2010delT) may result in OI.On the other hand, there have not been any studies investigating the association between previously mentioned COL5A1 gene polymorphisms and TMJ internal derangements, including ADDwoR.
1 COL5A1 UNIPROT:P20908 activates UNIPROT:P78504 Protein ec58cd60-f577-11eb-8f00-001a4a160176 32583079 After confirming that si-COL5A1s effectively downregulated COL5A1 by western blotting and qRT-PCR assay (Fig.5m, n), the CCK-8 assay was conducted, and the results showed that knockdown of COL5A1 greatly repressed the growth of AGS and HGC27 cells (Fig.5o).
1 COL5A1 UNIPROT:P20908 increases UNIPROT:P20908 Protein ec58cd60-f577-11eb-8f00-001a4a160176 32583079 In the present study, we found that HOTAIR and COL5A1 were overexpressed in GC cell lines and that overexpression of HOTAIR promoted the proliferation and metastasis of GC by sponging miR-1277-5p and upregulating COL5A1.
1 COL5A1 UNIPROT:P20908 increases GO:0031012 Phenotype 6b1ddcf8-8d8a-11e7-ad74-001a4ae51246 28683323 Importantly, the individual expression levels ofCOL1A1,COL1A2,COL5A1, andCOL5A2were significantly correlated with each other in patient glioma tumors from three independent clinical cohorts (Figure 2J;Figures S2L and S2M), suggestive of a common upstream mechanism driving concerted ECM collagen expression in glioma tumors.
1 COL5A1 UNIPROT:P20908 activates GO:0031012 Phenotype e0f1c4d0-bc26-11e5-8abe-001a4ae51246 PMC3742561 Both COL5A1 and COL5A2 produce different components of type V collagen, present in the skin, bones, ligaments, tendons, muscles, and the ECM[17].
1 COL5A1 UNIPROT:P20908 activates MESH:D000077192 Phenotype 743deed8-753a-11ee-add2-0050569a791b 10.1007/s10528-022-10307-3 High levels of COL5A1 have been shown to accelerate the progression and metastasis of breast cancer, lung adenocarcinoma, and gastric cancer (Liu et al.2018; Wei et al.2020b; Zhao et al.2020).
1 COL5A1 UNIPROT:P20908 activates GO:0070341 Phenotype ef8306fc-c474-11e5-9cc6-001a4ae51246 PMC4394244 "Our data show that in Plxnd1-deficient VAT, the induction of Col5a1 promotes adipocyte proliferation and differentiation,
leading to hyperplastic VAT morphology and reduced lipid accumulation."
1 COL5A1 UNIPROT:P20908 activates GO:0016477 Phenotype 0e9e3a84-5c1d-11e7-b441-001a4ae51247 PMC5396846 "COL11A1 and
COL5A1 promote cell migration and tumor progression in mice (50)."
1 COL5A1 UNIPROT:P20908 activates GO:0042060 Phenotype e1042f6a-3b32-11e9-8325-001a4a160175 PMC6369854 Compared with controls, wound healing was significantly inhibited by COL5A1 siRNA in Caki-1 cells (Figure 4A).
1 COL5A1 UNIPROT:P20908 inhibits GO:0008283 Phenotype 4e48ef5c-73a5-11ee-9572-0050569a1f61 10.1007/s12094-023-03270-x Downregulation of COL5A1 expression inhibits tumor cell proliferation and migration, and its expression levels are correlated with tumor immune infiltration, staging, and prognosis in various human cancers [44–46].
1 COL5A1 UNIPROT:P20908 inhibits GO:0008283 Phenotype 23705ecc-ae95-11ec-ae7b-0050569a1f61 PMCPMC8079757 The results showed that overexpression of COL5A1 could partially reverse the inhibition of cell proliferation and invasion by miR-582-5p.In addition, the upstream regulators such as transcription factors may be responsible for dysregulated expression of miRNAs in cancers.
1 COL5A1 UNIPROT:P20908 activates GO:0008283 Phenotype 743deed8-753a-11ee-add2-0050569a791b 10.1007/s10528-022-10307-3 COL5A1 was overexpressed in EC tissues and cells, and COL5A1 knockdown suppressed cell proliferation and promoted apoptosis in EC cells.
1 COL5A1 UNIPROT:P20908 activates MESH:D009369 Phenotype 23705ecc-ae95-11ec-ae7b-0050569a1f61 PMCPMC8079757 "In vivo, the decreased tumor size and weight by miR-582-5p were reversed by COL5A1 overexpression (
Figure 5E
)."
1 COL5A1 UNIPROT:P20908 activates MESH:D009369 Phenotype 689fc166-c6d7-11ee-b346-0050569a791b 10.1016/j.compbiomed.2023.107597 High COL5A1 expression can promote tumor metastasis or progression, and recent reports suggest that the COL5A1 gene in CAFs suppresses immune activation [78].
1 COL5A1 UNIPROT:P20908 activates MESH:D009369 Phenotype 3c866ebe-f616-11eb-b551-001a4a160175 PMC7079284 Increased levels of COL1A1, COL3A1, COL5A1, and PCOLCE are associated with cancer stem cells and increased tumor recurrence [122]; all were reduced with RA treatment in our study.
1 COL5A1 UNIPROT:P20908 activates MESH:D009369 Phenotype 0e9e3a84-5c1d-11e7-b441-001a4ae51247 PMC5396846 "COL11A1 and
COL5A1 promote cell migration and tumor progression in mice (50)."
1 COL5A1 UNIPROT:P20908 activates MESH:D009369 Phenotype ae3b46ac-ae95-11ec-ae7b-0050569a1f61 PMCPMC8147444 A previous study also showed that high expression of COL1A1, COL3A1, COL5A1, and COL5A2 in ovarian cancer promotes tumor immune tolerance and results in poor prognosis [53].
1 COL5A1 UNIPROT:P20908 inhibits GO:0006412 Phenotype 6d121918-ae94-11ec-ae7b-0050569a1f61 PMCPMC8283311 miRNA can inhibit protein synthesis by binding to COL5A1 3′-UTR to regulate target mRNA stability and/or translation efficiency (Garzon et al., 2009).
1 COL5A1 UNIPROT:P20908 activates MESH:D009362 Phenotype 689fc166-c6d7-11ee-b346-0050569a791b 10.1016/j.compbiomed.2023.107597 High COL5A1 expression can promote tumor metastasis or progression, and recent reports suggest that the COL5A1 gene in CAFs suppresses immune activation [78].
1 COL5A1 UNIPROT:P20908 activates MESH:D009362 Phenotype 1ce8f3ea-c68d-11ee-b346-0050569a791b 10.1016/j.pharmthera.2023.108576 Their study demonstrated that NAT10 can write ac4C modification in the 3′ UTR of COL5A1(Collagen type V Alpha 1 chain) mRNA, thereby enhancing the stability ofCOL5A1mRNA and promoting gastric cancer cell EMT(Epithelial-Mesenchymal transition) and metastasis (Zhang, Jing, Wang, et al., 2021a).
1 COL5A1 UNIPROT:P20908 activates MESH:D009362 Phenotype 743deed8-753a-11ee-add2-0050569a791b 10.1007/s10528-022-10307-3 High levels of COL5A1 have been shown to accelerate the progression and metastasis of breast cancer, lung adenocarcinoma, and gastric cancer (Liu et al.2018; Wei et al.2020b; Zhao et al.2020).
1 COL5A1 UNIPROT:P20908 activates MESH:D005355 Phenotype d95fdb8a-374e-11e8-8f56-001a4a160175 28028586 A computational integrative analysis found higher number of target genes involved in HSC activation and liver fibrosis such as different collagen types (Col5a1, Col4a5, Col8a1, Col9a3),Lox,TgfβorIL-6under the influence of miRNA expressed in quiescent HSC (qHSC) relative to their myofibroblast-like counterparts.
1 COL5A1 UNIPROT:P20908 activates MESH:D005355 Phenotype 940f8760-bc12-11e5-9b9d-001a4ae51247 PMC4476106 Importantly, miRNAs expressed in qHSCs targeted genes involved in HSC activation and liver fibrosis such as different collagen types (COL5A1,COL4A5, COL8A1, COL9A3),LOX,TGFβorIL-612030.
1 COL5A1 UNIPROT:P20908 inhibits GO:0007155 Phenotype 15163a70-8df9-11e7-b4f4-001a4ae51246 27266404 The adhesion molecules that are down-regulated by GDNF includeCdh13,Col5a1,Fibronectin-1,Reelin,Thrombospondin 1and4, andVcam1.
1 COL5A1 UNIPROT:P20908 activates GO:0030154 Phenotype ef8306fc-c474-11e5-9cc6-001a4ae51246 PMC4394244 "Our data show that in Plxnd1-deficient VAT, the induction of Col5a1 promotes adipocyte proliferation and differentiation,
leading to hyperplastic VAT morphology and reduced lipid accumulation."
1 COL5A1 UNIPROT:P20908 activates MESH:D051379 Phenotype 0e9e3a84-5c1d-11e7-b441-001a4ae51247 PMC5396846 "COL11A1 and
COL5A1 promote cell migration and tumor progression in mice (50)."
1 COL5A1 UNIPROT:P20908 inhibits MESH:D051379 Phenotype 17a1c830-c46b-11e5-8491-001a4ae51247 25122555 "Col5a1+/−mice also have decreased tendon stiffness, which is primarily due to a smaller tendon cross-sectional area (CSA) compared
with that of control mice (8)."
1 COL5A1 UNIPROT:P20908 activates GO:0006915 Phenotype 743deed8-753a-11ee-add2-0050569a791b 10.1007/s10528-022-10307-3 COL5A1 was overexpressed in EC tissues and cells, and COL5A1 knockdown suppressed cell proliferation and promoted apoptosis in EC cells.
1 COL5A1 UNIPROT:P20908 activates GO:0006915 Phenotype 23705ecc-ae95-11ec-ae7b-0050569a1f61 PMCPMC8079757 Previous study by Feng G et al. has found COL5A1 promoted ccRCC cell proliferation, apoptosis, migration, invasion in vitro (32).
1 COL5A1 UNIPROT:P20908 activates GO:0006915 Phenotype 7ddb759e-cc0f-11ec-99c8-0050569a791b PMC7773178 bSep08, Col5a1, aSep0, soygee.aSep08-unspliced, NONRATT013247.2, votar.aSep08-unspliced, etc, both participate in and mediate the process of inflammatory response, cell apoptosis.
1 COL5A1 UNIPROT:P20908 activates GO:0006954 Phenotype 7ddb759e-cc0f-11ec-99c8-0050569a791b PMC7773178 bSep08, Col5a1, aSep0, soygee.aSep08-unspliced, NONRATT013247.2, votar.aSep08-unspliced, etc, both participate in and mediate the process of inflammatory response, cell apoptosis.
1 COL5A1 UNIPROT:P20908 inhibits MESH:D003094 Phenotype 06f3364c-bc35-11e5-ac4e-001a4ae51246 PMC4470940 Tissue inhibitor of metalloproteinase 1 and 2 (TIMP1 and TIMP2), and collagen alpha-I (V) chain precursor (COL5A1) were indirectly connected through matrix metalloproteinase 2 (MMP2) protein.
1 COL5A1 UNIPROT:P20908 activates MESH:D003094 Phenotype 64a9f84e-38d7-11e9-87c2-001a4a160175 30791866 Mutations in COL5A1 and COL3A1 also promote collagen retention in the cytoplasm [89].
1 COL5A1 UNIPROT:P20908 activates MESH:D003094 Phenotype fedad284-97c5-11e8-b8fa-001a4a160176 PMC6070246 Within the network of post-translational modification, BDE-99 also up-regulated a series of genes involved in protein degradation such as serine protease, trypsinogen, and chymotrypsin, but down-regulated many collagen-related protein synthesis, such as collagen type V alpha 1 chain (Col5a1), Col3a1, ERBB receptor feedback inhibitor 1 (Errfl1),serpin family H member 1 (Serpinh1), and phospholipase C beta 3 (Plcb3).
1 COL5A1 UNIPROT:P20908 increases MESH:D003094 Phenotype 6b1ddcf8-8d8a-11e7-ad74-001a4ae51246 28683323 Importantly, the individual expression levels ofCOL1A1,COL1A2,COL5A1, andCOL5A2were significantly correlated with each other in patient glioma tumors from three independent clinical cohorts (Figure 2J;Figures S2L and S2M), suggestive of a common upstream mechanism driving concerted ECM collagen expression in glioma tumors.
1 COL5A1 UNIPROT:P20908 activates GO:0016049 Phenotype e1042f6a-3b32-11e9-8325-001a4a160175 PMC6369854 MTT assay showed that COL5A1 knockdown inhibited cell growth in a time-dependent manner compared with controls (Figure 3B).
1 COL5A1 UNIPROT:P20908 activates MESH:D004535 Phenotype 4f7085b6-2ab2-11e9-95a4-001a4a160175 PMC6361458 Classical Ehlers-Danlos syndrome (cEDS) is a dominant inherited connective tissue disorder mainly caused by mutations in the COL5A1 and COL5A2 genes encoding type V collagen (COLLV), which is a fibrillar COLL widely distributed in a variety of connective tissues.
1 COL5A1 UNIPROT:P20908 activates MESH:D012008 Phenotype 3c866ebe-f616-11eb-b551-001a4a160175 PMC7079284 Increased levels of COL1A1, COL3A1, COL5A1, and PCOLCE are associated with cancer stem cells and increased tumor recurrence [122]; all were reduced with RA treatment in our study.
1 COL5A1 UNIPROT:P20908 activates MESH:D002292 Phenotype ec58cd60-f577-11eb-8f00-001a4a160176 32583079 In addition, a high level of COL5A1 accelerates the growth and progression of renal cell carcinoma and breast cancer [37,38], which reminds us that ECM may play an important role in GC.
1 COL5A1 UNIPROT:P20908 activates MESH:D002292 Phenotype f228d508-8280-11ee-add2-0050569a791b 10.1007/s12020-022-03175-9 In addition, high levels of COL5A1 accelerate the growth and progression in renal cell carcinoma and breast cancer [26,27].
1 COL5A1 UNIPROT:P20908 activates FPLX:COL5 ProteinFamily e0f1c4d0-bc26-11e5-8abe-001a4ae51246 PMC3742561 Both COL5A1 and COL5A2 produce different components of type V collagen, present in the skin, bones, ligaments, tendons, muscles, and the ECM[17].
1 COL5A1 UNIPROT:P20908 activates FPLX:COL5 ProteinFamily 4f7085b6-2ab2-11e9-95a4-001a4a160175 PMC6361458 Classical Ehlers-Danlos syndrome (cEDS) is a dominant inherited connective tissue disorder mainly caused by mutations in the COL5A1 and COL5A2 genes encoding type V collagen (COLLV), which is a fibrillar COLL widely distributed in a variety of connective tissues.
1 COL5A1 UNIPROT:P20908 inhibits FPLX:CD8 ProteinFamily f228d508-8280-11ee-add2-0050569a791b 10.1007/s12020-022-03175-9 The expression of COL11A1 and COL5A1 significantly downregulated CD8 cells infiltration and upregulated Treg cell infiltration (Fig.6A).
1 UNIPROT:P03372 activates COL5A1 UNIPROT:P20908 Protein 98a0c24c-c47a-11e5-85e4-001a4ae51246 PMC3182741 In females, by contrast, antagonism of ER with fulvestrant significantly increased the relative expression ofIhh, Col4a2, Col5a1, Col6a2, andCol14a1, but decreasedFgf3, Msx1, Igfbp2, andIgfbp5(Fig. 5andTable S1).
1 UNIPROT:Q9UQB3 inhibits COL5A1 UNIPROT:P20908 Protein 6a076404-bc23-11e5-8abe-001a4ae51246 10.1016/j.ejca.2012.06.024 hSecT60A induced gene expression of MMP7, MMP9, MMP13, NCAM1, LAMA3, CTNND2, CDH1, LAMB3, TGFB-1, ADAMTS1 and ITGA8, and repressed COL12A1, COL5A1, ITGB5, FN1, LAMB1, CTGF, ITGB2, SELP, ITGA7, ITGA4, ITGB4, MMP12, MMP14, ECM1 and ADAMTS8 (Supplementary data).
1 FPLX:Notch activates COL5A1 UNIPROT:P20908 ProteinFamily d2f03c90-c6f9-11ee-9133-0050569a1f61 10.1016/j.bbrc.2023.09.048 Notch signaling-activated RBPJ transcribes the collagen V genes (Col5a1/Col5a3) in MuSCs, thereby depositing collagen V protein under the basal lamina.
1 PUBCHEM:11655119 inhibits COL5A1 UNIPROT:P20908 Chemical 26c5c27e-c47c-11e5-a92e-001a4ae51246 22006998 "Immunohistochemical staining
showed that LY2109761 alone and in combination with radiotherapy reduced the expression of established mesenchymal marker
proteins including fibronectin, COL5A1, and YKL-40 (refs.23, 25;Fig. 7B)."
1 GO:0010467 inhibits COL5A1 UNIPROT:P20908 Phenotype 6a076404-bc23-11e5-8abe-001a4ae51246 10.1016/j.ejca.2012.06.024 hSecT60A induced gene expression of MMP7, MMP9, MMP13, NCAM1, LAMA3, CTNND2, CDH1, LAMB3, TGFB-1, ADAMTS1 and ITGA8, and repressed COL12A1, COL5A1, ITGB5, FN1, LAMB1, CTGF, ITGB2, SELP, ITGA7, ITGA4, ITGB4, MMP12, MMP14, ECM1 and ADAMTS8 (Supplementary data).
1 UNIPROT:P14780 inhibits COL5A1 UNIPROT:P20908 Protein 6a076404-bc23-11e5-8abe-001a4ae51246 10.1016/j.ejca.2012.06.024 hSecT60A induced gene expression of MMP7, MMP9, MMP13, NCAM1, LAMA3, CTNND2, CDH1, LAMB3, TGFB-1, ADAMTS1 and ITGA8, and repressed COL12A1, COL5A1, ITGB5, FN1, LAMB1, CTGF, ITGB2, SELP, ITGA7, ITGA4, ITGB4, MMP12, MMP14, ECM1 and ADAMTS8 (Supplementary data).
1 UNIPROT:P11161 activates COL5A1 UNIPROT:P20908 Protein f6da1e5e-c479-11e5-91a7-001a4ae51247 PMC3081194 Results showed that Col5A1 was induced by overexpression of Egr-2 in both normal adult or SSc fibroblasts (seeSupplemental Figure S3athttp://ajp.amjpathol.org); the effect was similar compared with normal foreskin fibroblasts.
1 UNIPROT:P01308 activates COL5A1 UNIPROT:P20908 Protein 2cb9a202-bc45-11e5-ac4e-001a4ae51246 PMC2839497 Insulin induced a clear increase of the mature form of COL1A1, of a COL5A1 fragment, and of the C-terminal peptides of COL1A1, COL1A2, and COL3A1.
1 UNIPROT:P12830 inhibits COL5A1 UNIPROT:P20908 Protein 6a076404-bc23-11e5-8abe-001a4ae51246 10.1016/j.ejca.2012.06.024 hSecT60A induced gene expression of MMP7, MMP9, MMP13, NCAM1, LAMA3, CTNND2, CDH1, LAMB3, TGFB-1, ADAMTS1 and ITGA8, and repressed COL12A1, COL5A1, ITGB5, FN1, LAMB1, CTGF, ITGB2, SELP, ITGA7, ITGA4, ITGB4, MMP12, MMP14, ECM1 and ADAMTS8 (Supplementary data).
1 MESH:D003907 decreases COL5A1 UNIPROT:P20908 Phenotype 689fc166-c6d7-11ee-b346-0050569a791b 10.1016/j.compbiomed.2023.107597 Dexamethasone, a glucocorticoid drug commonly used in the treatment of multiple myeloma, exhibited high-affinity docking binding energy and down-regulated COL5A1 expression.
1 MESH:D020123 decreases COL5A1 UNIPROT:P20908 Phenotype 1d29d17e-3531-11e8-8636-001a4a160175 24630239 Taken together with the evidence that rapamycin suppressed mRNA levels of COL3A1 and COL5A1 genes, while not those of fibronectin, tenascin C and tissue inhibitor of metalloproteinase 1 genes in SSc dermal fibroblasts (supplementary Fig. 1), it is likely that the activation of mTOR is largely involved in the regulation of fibrillar collagen (types I, III and V) and MMP1 and rapamycin reverses the altered expression of these genes in SSc dermal fibroblasts.
1 UNIPROT:P45452 inhibits COL5A1 UNIPROT:P20908 Protein 6a076404-bc23-11e5-8abe-001a4ae51246 10.1016/j.ejca.2012.06.024 hSecT60A induced gene expression of MMP7, MMP9, MMP13, NCAM1, LAMA3, CTNND2, CDH1, LAMB3, TGFB-1, ADAMTS1 and ITGA8, and repressed COL12A1, COL5A1, ITGB5, FN1, LAMB1, CTGF, ITGB2, SELP, ITGA7, ITGA4, ITGB4, MMP12, MMP14, ECM1 and ADAMTS8 (Supplementary data).
1 UNIPROT:P01137 inhibits COL5A1 UNIPROT:P20908 Protein 6a076404-bc23-11e5-8abe-001a4ae51246 10.1016/j.ejca.2012.06.024 hSecT60A induced gene expression of MMP7, MMP9, MMP13, NCAM1, LAMA3, CTNND2, CDH1, LAMB3, TGFB-1, ADAMTS1 and ITGA8, and repressed COL12A1, COL5A1, ITGB5, FN1, LAMB1, CTGF, ITGB2, SELP, ITGA7, ITGA4, ITGB4, MMP12, MMP14, ECM1 and ADAMTS8 (Supplementary data).
1 UNIPROT:P13591 inhibits COL5A1 UNIPROT:P20908 Protein 6a076404-bc23-11e5-8abe-001a4ae51246 10.1016/j.ejca.2012.06.024 hSecT60A induced gene expression of MMP7, MMP9, MMP13, NCAM1, LAMA3, CTNND2, CDH1, LAMB3, TGFB-1, ADAMTS1 and ITGA8, and repressed COL12A1, COL5A1, ITGB5, FN1, LAMB1, CTGF, ITGB2, SELP, ITGA7, ITGA4, ITGB4, MMP12, MMP14, ECM1 and ADAMTS8 (Supplementary data).
1 UNIPROT:Q13751 inhibits COL5A1 UNIPROT:P20908 Protein 6a076404-bc23-11e5-8abe-001a4ae51246 10.1016/j.ejca.2012.06.024 hSecT60A induced gene expression of MMP7, MMP9, MMP13, NCAM1, LAMA3, CTNND2, CDH1, LAMB3, TGFB-1, ADAMTS1 and ITGA8, and repressed COL12A1, COL5A1, ITGB5, FN1, LAMB1, CTGF, ITGB2, SELP, ITGA7, ITGA4, ITGB4, MMP12, MMP14, ECM1 and ADAMTS8 (Supplementary data).
1 UNIPROT:Q16363 inhibits COL5A1 UNIPROT:P20908 Protein 6a076404-bc23-11e5-8abe-001a4ae51246 10.1016/j.ejca.2012.06.024 hSecT60A induced gene expression of MMP7, MMP9, MMP13, NCAM1, LAMA3, CTNND2, CDH1, LAMB3, TGFB-1, ADAMTS1 and ITGA8, and repressed COL12A1, COL5A1, ITGB5, FN1, LAMB1, CTGF, ITGB2, SELP, ITGA7, ITGA4, ITGB4, MMP12, MMP14, ECM1 and ADAMTS8 (Supplementary data).
1 UNIPROT:P17676 increases COL5A1 UNIPROT:P20908 Protein da3a1a06-f58c-11eb-9545-001a4a160176 30072121 "Moreover, knockdown of STAT3 and C/EBPβ reduced fibronectin and COL5A1 protein expression in SNB-19 tumors in NOD/SCID mice [74]."
1 HGNC:31532 activates COL5A1 UNIPROT:P20908 Protein a0a2068a-351c-11e8-b868-001a4a160176 28527972 Increased levels of miR-145 may cause downregulation of collagen type V alpha (COL5A1) expression.
1 UNIPROT:Q9H0A0 increases COL5A1 UNIPROT:P20908 Protein 81838fc4-89a0-11ee-ae93-0050569a1f61 10.1007/s12032-022-01736-6 NAT10 can promote the metastasis of gastric cancer by upregulating the ac4C modification level of COL5A1 mRNA [15].
1 UNIPROT:Q9H0A0 actelytatesProtein COL5A1 UNIPROT:P20908 Protein e07badee-c691-11ee-b346-0050569a791b 10.1016/j.prp.2023.154990 Zhang et al. found in 2021 that NAT10 may promote gastric cancer metastasis by acetylating COL5A1 via ac4C[66].
1 UNIPROT:Q9H0A0 activates COL5A1 UNIPROT:P20908 Protein 3f6e5e0c-76d6-11ee-add2-0050569a791b 10.1007/s10555-023-10120-3 For instance, in gastric cancer, NAT10 promotes metastasis and EMT by targeting COL5A1 mRNA and increasing its stability [292].
1 MESH:D005938 decreases COL5A1 UNIPROT:P20908 Phenotype 689fc166-c6d7-11ee-b346-0050569a791b 10.1016/j.compbiomed.2023.107597 Dexamethasone, a glucocorticoid drug commonly used in the treatment of multiple myeloma, exhibited high-affinity docking binding energy and down-regulated COL5A1 expression.
1 UNIPROT:Q8TDD2 increases COL5A1 UNIPROT:P20908 Protein aeff1be6-390e-11e8-9fbf-001a4a160176 27498006 Previous studies have demonstrated that Osterix enhances the expression of Col5a1 and Col5a3 genes, contributing to osteoblast differentiation[4,5].
1 UNIPROT:P40763 increases COL5A1 UNIPROT:P20908 Protein da3a1a06-f58c-11eb-9545-001a4a160176 30072121 "Moreover, knockdown of STAT3 and C/EBPβ reduced fibronectin and COL5A1 protein expression in SNB-19 tumors in NOD/SCID mice [74]."
1 MESH:D000485 increases COL5A1 UNIPROT:P20908 Phenotype 24d361b0-ae95-11ec-b4ed-0050569a1f61 PMCPMC8229663 However, allergen-activated eosinophils did not affect COL5A1 gene expression in ASMC and PF cells.
1 UNIPROT:Q01196 decreases COL5A1 UNIPROT:P20908 Protein 23705ecc-ae95-11ec-ae7b-0050569a1f61 PMCPMC8079757 Over-expression of RUNX1 led to decreased miR-582-5p expression and increased COL5A1 expression, which demonstrates that there is an axis among RUNX1/miR-582-5p/COL5A1 signaling.
1 UNIPROT:Q01196 inhibits COL5A1 UNIPROT:P20908 Protein 5386d36a-bd7b-11ee-a53a-0050569a1f61 10.1007/s00210-024-02960-9 Xue et al. (45) indicated that the RUNX1/miR-582-5p suppressed the growth and migration of clear cell renal cell carcinoma by targeting COL5A1.
1 UNIPROT:P09237 inhibits COL5A1 UNIPROT:P20908 Protein 6a076404-bc23-11e5-8abe-001a4ae51246 10.1016/j.ejca.2012.06.024 hSecT60A induced gene expression of MMP7, MMP9, MMP13, NCAM1, LAMA3, CTNND2, CDH1, LAMB3, TGFB-1, ADAMTS1 and ITGA8, and repressed COL12A1, COL5A1, ITGB5, FN1, LAMB1, CTGF, ITGB2, SELP, ITGA7, ITGA4, ITGB4, MMP12, MMP14, ECM1 and ADAMTS8 (Supplementary data).
1 UNIPROT:O00592 increases COL5A1 UNIPROT:P20908 Protein 2957cc06-bbd2-11e5-956b-001a4ae51247 PMC3726015 Further examination of the microarray data indicated that the expression of collagen type V, alpha 1 (COL5A1; 1.52-fold change) and collagen type V, alpha 2 (COL5A2; 1.44-fold change) was also upregulated by PC although the changes were less than 1.6-fold (Table 2).
1 UNIPROT:Q9UHI8 inhibits COL5A1 UNIPROT:P20908 Protein 6a076404-bc23-11e5-8abe-001a4ae51246 10.1016/j.ejca.2012.06.024 hSecT60A induced gene expression of MMP7, MMP9, MMP13, NCAM1, LAMA3, CTNND2, CDH1, LAMB3, TGFB-1, ADAMTS1 and ITGA8, and repressed COL12A1, COL5A1, ITGB5, FN1, LAMB1, CTGF, ITGB2, SELP, ITGA7, ITGA4, ITGB4, MMP12, MMP14, ECM1 and ADAMTS8 (Supplementary data).
1 HGNC:33510 increases COL5A1 UNIPROT:P20908 Protein ec58cd60-f577-11eb-8f00-001a4a160176 32583079 Taken together, these findings elucidated that HOTAIR upregulated COL5A1 expression by sponging miR-1277-5p to promote the progression of GC, and intervening collagen (COL5A1) expression by lncRNAs may provide new insights into the treatment of GC.
1 HGNC:33510 activates COL5A1 UNIPROT:P20908 Protein ec58cd60-f577-11eb-8f00-001a4a160176 32583079 Taken together, we could conclude that HOTAIR upregulated COL5A1 by sponging miR-1277-5p, which disrupted the normal ECM to change the GC microenvironment, promoting immune infiltration, proliferation and metastasis of GC (Fig.6g).
1 UNIPROT:P53708 inhibits COL5A1 UNIPROT:P20908 Protein 6a076404-bc23-11e5-8abe-001a4ae51246 10.1016/j.ejca.2012.06.024 hSecT60A induced gene expression of MMP7, MMP9, MMP13, NCAM1, LAMA3, CTNND2, CDH1, LAMB3, TGFB-1, ADAMTS1 and ITGA8, and repressed COL12A1, COL5A1, ITGB5, FN1, LAMB1, CTGF, ITGB2, SELP, ITGA7, ITGA4, ITGB4, MMP12, MMP14, ECM1 and ADAMTS8 (Supplementary data).
1 UNIPROT:P20908 increases COL5A1 UNIPROT:P20908 Protein ec58cd60-f577-11eb-8f00-001a4a160176 32583079 In the present study, we found that HOTAIR and COL5A1 were overexpressed in GC cell lines and that overexpression of HOTAIR promoted the proliferation and metastasis of GC by sponging miR-1277-5p and upregulating COL5A1.