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Overexpression of miR‐623 suppresses progression of hepatocellular carcinoma via regulating the PI3K/Akt signaling pathway by targeting XRCC5
Author(s) -
Ren Feng,
Su Hui,
Jiang Haitao,
Chen Yunjie
Publication year - 2020
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.29117
Subject(s) - wnt signaling pathway , protein kinase b , pi3k/akt/mtor pathway , downregulation and upregulation , mapk/erk pathway , cancer research , kinase , signal transduction , cell growth , biology , microbiology and biotechnology , chemistry , biochemistry , gene
It has been reported that miR‐623 is deregulated in lung adenocarcinoma and inhibits tumor growth and invasion. However, it is unclear whether miR‐623 has a role in the progression of hepatocellular carcinoma (HCC). Herein, we found that miR‐623 was significantly downregulated in HCC, and that its expression was related to poor clinical outcomes of patients with HCC. Upregulation of miR‐623 decreased cell proliferation, viability, migration, and invasion and further promoted apoptosis in 7721, Huh7, and Bel‐7402 cells. Moreover, we also observed that miR‐623 regulated the phosphoinositide 3‐kinase/protein kinase B (PI3K/Akt), Wnt/β‐catenin, and extracellular regulated protein kinases/c‐Jun N‐terminal kinase (ERK/JNK) signaling pathways as well as the expression level of related proteins. Further, X‐ray repair cross complementing 5 ( XRCC5 ) was a direct target for miR‐623, and the suppression of PI3K/Akt, Wnt/β‐catenin, and ERK/JNK signaling pathways and cell proliferation and invasion abilities caused by miR‐623 in HCC cells was significantly reversed by the upregulation of XRCC5 . Collectively, our data suggested that miR‐623 suppressed the progression of HCC by regulating the PI3K/Akt, Wnt/β‐catenin, and ERK/JNK pathways by targeting XRCC5 in HCC in vitro, indicating that miR‐623 may be a target for the therapy of HCC.