Open AccessPLCA8 suppresses breast cancer apoptosis by activating the PI3k/AKT/NF‐κB pathway
Author(s) -
Mao Misha,
Chen Yongxia,
Jia Yunlu,
Yang Jingjing,
Wei Qun,
Li Zhaoqing,
Chen Lini,
Chen Cong,
Wang Linbo
Publication year - 2019
Publication title -
journal of cellular and molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.44
H-Index - 130
eISSN - 1582-4934
pISSN - 1582-1838
DOI - 10.1111/jcmm.14578
Subject(s) - pi3k/akt/mtor pathway , protein kinase b , apoptosis , biology , gene silencing , cancer research , cell growth , microbiology and biotechnology , signal transduction , cancer cell , vimentin , cell , cancer , immunology , immunohistochemistry , gene , biochemistry , genetics
The cysteine‐rich lysosomal protein placenta‐specific 8 (PLAC8), also called onzin, has been shown to be involved in many types of cancers, and its role is highly dependent on cellular and physiological contexts. However, the precise function of PLAC8 in breast cancer (BC) progression remains unclear. In this study, we investigated both the clinical significance and biological functions of PLAC8 in BC progression. First, high PLAC8 expression was observed in primary BC tissues compared with adjacent normal tissues through immunohistochemistry analysis. The results of in vitro and in vivo assays further confirmed that PLAC8 overexpression promotes cell proliferation and suppress BC cell apoptosis, whereas PLAC8 silencing has the opposite effect. In addition, the forced expression of PLAC8 greatly induces cell migration, partially by affecting the EMT‐related genes, including down‐regulating E‐cadherin expression and facilitating vimentin expression. Further mechanistic analysis confirmed that PLAC8 contributes to cell proliferation and suppresses cell apoptosis in BC by activating the PI3K/AKT/NF‐κB pathway. The results of our study provide new insights into an oncogenic role of PLAC8 and reveal a novel PLAC8/ PI3K/AKT/NF‐κB pathway as a potential therapeutic target for BC.