TNFAIP8 regulates gastric cancer growth via mTOR-Akt-ULK1 pathway and autophagy signals.

TNFAIP8 regulates gastric cancer growth via mTOR-Akt-ULK1 pathway and autophagy signals.
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DOI:
10.1111/jcmm.16413
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发表时间:
2021-04
影响因子:
5.3
通讯作者:
Chen Y
Chen Y
中科院分区:
医学2区
文献类型:
--
作者:
Chen Z;Zhang J;Dong C;Li D;Yin Y;Yu W;Chen Y

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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.
TNFAIP8通过MDM2/p53通路促进非小细胞肺癌的增殖和顺铂化疗耐药。
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