Upregulation of Excision Repair Cross-Complementation Group 6-Like (ERCC6L) Promotes Tumor Growth in Hepatocellular Carcinoma.
Apoptosis
Carcinoma, Hepatocellular
/ metabolism
Cell Line, Tumor
Cell Proliferation
/ physiology
DNA Helicases
/ genetics
Gene Expression Regulation, Neoplastic
Gene Knockdown Techniques
Humans
Liver Neoplasms
/ metabolism
Prognosis
Signal Transduction
Tumor Suppressor Protein p53
/ metabolism
Up-Regulation
Cell cycle
ERCC6L
Hepatocellular carcinoma
Proliferation
p53 signaling
Journal
Digestive diseases and sciences
ISSN: 1573-2568
Titre abrégé: Dig Dis Sci
Pays: United States
ID NLM: 7902782
Informations de publication
Date de publication:
04 2021
04 2021
Historique:
received:
16
12
2019
accepted:
16
04
2020
pubmed:
30
4
2020
medline:
19
8
2021
entrez:
30
4
2020
Statut:
ppublish
Résumé
Excision repair cross-complementation group 6-like (ERCC6L) is overexpressed in some malignancies; however, its role in hepatocellular carcinoma (HCC) remains to be further investigated. In the present study, we explored the expression and function of ERCC6L in HCC. We investigated the expression of ERCC6L by microarray analysis, using the Cancer Genome Atlas database, and by HCC tissue microarray. The results showed that ERCC6L expression was upregulated in tumor specimens and HCC cell lines. High ERCC6L expression in tumor tissues was significantly correlated with poor prognosis and could serve as an independent prognostic indicator for HCC patients. Results of in vitro and in vivo assays revealed that ERCC6L substantially promoted cell proliferation, and our flow cytometry analysis revealed that this was accomplished by acceleration of the G1/S transition. Finally, gene set enrichment analysis and western blotting results indicated that ERCC6L might regulate HCC proliferation by activating p53 signaling. Our study suggests that ERCC6L plays an important role in HCC proliferation and that it might serve as a promising therapeutic target in HCC.
Sections du résumé
BACKGROUND
Excision repair cross-complementation group 6-like (ERCC6L) is overexpressed in some malignancies; however, its role in hepatocellular carcinoma (HCC) remains to be further investigated.
AIMS
In the present study, we explored the expression and function of ERCC6L in HCC.
METHODS AND RESULTS
We investigated the expression of ERCC6L by microarray analysis, using the Cancer Genome Atlas database, and by HCC tissue microarray. The results showed that ERCC6L expression was upregulated in tumor specimens and HCC cell lines. High ERCC6L expression in tumor tissues was significantly correlated with poor prognosis and could serve as an independent prognostic indicator for HCC patients. Results of in vitro and in vivo assays revealed that ERCC6L substantially promoted cell proliferation, and our flow cytometry analysis revealed that this was accomplished by acceleration of the G1/S transition. Finally, gene set enrichment analysis and western blotting results indicated that ERCC6L might regulate HCC proliferation by activating p53 signaling.
CONCLUSIONS
Our study suggests that ERCC6L plays an important role in HCC proliferation and that it might serve as a promising therapeutic target in HCC.
Identifiants
pubmed: 32347436
doi: 10.1007/s10620-020-06277-4
pii: 10.1007/s10620-020-06277-4
doi:
Substances chimiques
Tumor Suppressor Protein p53
0
DNA Helicases
EC 3.6.4.-
ERCC6L protein, human
EC 3.6.4.12
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
1097-1109Subventions
Organisme : National Natural Science Foundation of China (CN)
ID : 81760497
Organisme : National Natural Science Foundation of China
ID : 81960446
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