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Downregulation of CLDN6 inhibits cell proliferation, migration, and invasion via regulating EGFR/AKT/mTOR signalling pathway in hepatocellular carcinoma
Author(s) -
Huang Lingyuan,
Zhao Chanjuan,
Sun Kai,
Yang Dandan,
Yan Linxia,
Luo Dan,
He Jinli,
Hu Xuemei,
Wang Rong,
Shen Xiaofei,
Xiao Ning,
Zhong Zhendong
Publication year - 2020
Publication title -
cell biochemistry and function
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.933
H-Index - 61
eISSN - 1099-0844
pISSN - 0263-6484
DOI - 10.1002/cbf.3489
Subject(s) - downregulation and upregulation , pi3k/akt/mtor pathway , cancer research , protein kinase b , gene silencing , cell growth , oncogene , biology , signal transduction , cell , microbiology and biotechnology , cell cycle , gene , biochemistry , genetics
Accumulating evidence showed that the claudin‐6 (CLDN6) expression was abnormal in many cancers, while its expression and biological functions in hepatocellular carcinoma (HCC) is still unclear. The present study demonstrated that CLDN6 was upregulated in HCC tissues compared with tumour‐adjacent tissues. CLDN6 silencing was significantly inhibited proliferation, migration, and invasion of HepG2 cells. Meanwhile, downregulation of CLDN6 remarkably inhibited the activation of EGFR/AKT/mTOR signalling pathway. Interestingly, the effect of CLDN6 overexpression on HepG2 cell proliferation and invasion could be inhibited by EGFR/AKT/mTOR signalling pathway inhibitor (AG1478). Significance of the study These findings suggested that CLDN6 may act as an oncogene in HCC and improve HepG2 cell proliferation, migration, and invasion may via EGFR/AKT/mTOR signalling pathway.