SEC61G plays an oncogenic role in hepatocellular carcinoma cells

Cell Cycle. 2020 Dec;19(23):3348-3361. doi: 10.1080/15384101.2020.1843816. Epub 2020 Nov 10.

Abstract

Hepatocellular carcinoma (HCC) is one of the most aggressive malignant diseases and requires more effective prevention and treatment strategies. Mutations or overexpression of endoplasmic reticulum (ER) proteins have been frequently identified in a solid tumor, suggesting that ER proteins play an important role in tumor development. SEC61G, a component of Sec61 complex located in the membrane of the human ER, has been revealed a potential relevance in glioblastoma multiforme. Analyses from TCGA database showed that SEC61G was overexpressed in HCC. Additionally, the expression of SEC61G mRNA was associated with the survival time of HCC patients. We verified that the higher expression of SEC61G in HCC tissues than paracancerous tissues. Moreover, knockdown of SEC61G inhibited cell proliferation and induced cell apoptosis in vitro. Besides, SEC61G was required for cell migration and invasion, conferring a potential role for SEC61G in tumor transfer. Taken together, our results revealed the role of SEC61G in HCC cells. Further detailed understanding of the signaling networks underlying SEC61G involvement in HCC cells would make SEC61G as a viable therapeutic target for pharmaceutical intervention of HCC.

Keywords: Hepatocellular carcinoma (HCC); SEC61G; Sec61 complex.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Carcinogenesis / genetics
  • Carcinogenesis / metabolism
  • Carcinoma, Hepatocellular / genetics
  • Carcinoma, Hepatocellular / metabolism*
  • Carcinoma, Hepatocellular / mortality
  • Gene Expression Regulation, Neoplastic / physiology*
  • Hep G2 Cells
  • Humans
  • Liver Neoplasms / genetics
  • Liver Neoplasms / metabolism*
  • Liver Neoplasms / mortality
  • Oncogenes / physiology*
  • SEC Translocation Channels / biosynthesis*
  • SEC Translocation Channels / genetics
  • Survival Rate / trends

Substances

  • SEC Translocation Channels
  • SEC61G protein, human

Grants and funding

This work was supported by the National Natural Science Foundation of China under Grant number 81602129; and the Natural Science Foundation of Shandong Province under Grant number ZR2016HB13.