Guangcong Zhang1, Jiamei Ma1, Ju Xiong2, Xiaoxi Huang1, Xiangyang Han3, Xiangnan Yu4, Xuemei Jiang5,6. 1. Department of Gastroenterology, Central South University Xiangya School of Medicine Affiliated Haikou Hospital, Haikou, 570100, China. 2. Department of Hepatobiliary Surgery, Hainan General Hospital, Haikou, 570100, China. 3. Department of Gastroenterology, Hainan General Hospital, Haikou, 570100, China. 4. Department of Gastroenterology and Hepatology, Zhongshan Hospital of Fudan University, Shanghai, 200030, China. 5. Department of Gastroenterology, Central South University Xiangya School of Medicine Affiliated Haikou Hospital, Haikou, 570100, China. jiang.xm18@foxmail.com. 6. Department of Gastroenterology, Hainan General Hospital, Haikou, 570100, China. jiang.xm18@foxmail.com.
Abstract
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.
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.
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