Open AccessTNFAIP8 regulates gastric cancer growth via mTOR‐Akt‐ULK1 pathway and autophagy signals
Author(s) -
Chen Zheng,
Zhang Jianguo,
Dong Chenyang,
Li Dongsheng,
Yin Yuehan,
Yu Wenhai,
Chen Yuezhi
Publication year - 2021
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.16413
Subject(s) - pi3k/akt/mtor pathway , autophagy , viability assay , protein kinase b , apoptosis , gene silencing , cancer research , flow cytometry , cell growth , cell , biology , chemistry , signal transduction , microbiology and biotechnology , biochemistry , gene
In this study, the purpose of this study was to investigate the role of TNFAIP8 in gastric cancer (GC). The expression of TNFAIP8 was detected by RT‐PCR or western blot . TNFAIP8 was silenced or overexpressed in two cell lines. CCK‐8 assay, transwell assay and flow cytometry were used to analyse cell viability, cell invasion capability and apoptosis, respectively. Nude mice were inoculated with TNFAIP8 silencing or overexpressing cells to form transplanted tumours. HE staining and immunohistochemistry assay were performed to assess histopathological changes in tumours. We found that the mRNA and protein expression of TNFAIP8 were significantly up‐regulated in GC tumour tissues and cells compared with the normal counterparts. Overexpression of TNFAIP8 in GC cells increased cell viability, decreased apoptosis and promoted the cell migration ability. Meanwhile, increased expression of TNFAIP8 promoted autophagy, while inhibiting mTOR‐Akt‐ULK1 signal pathway. In conclusions, this study presents data that TNFAIP8 inhibits GC cells presumably by down‐regulating mTOR‐Akt‐ULK1 signal pathway and activating autophagy signal.