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PIK3CB 通过 PI3K/AKT/mTOR 信号通路促进食管癌增殖。

PIK3CB promotes oesophageal cancer proliferation through the PI3K/AKT/mTOR signalling axis.

机构信息

Department of Thoracic Surgery, Chongqing University Cancer Hospital, Chongqing, China.

出版信息

Cell Biol Int. 2022 Sep;46(9):1399-1408. doi: 10.1002/cbin.11847. Epub 2022 Jul 16.

DOI:10.1002/cbin.11847
PMID:35842767
Abstract

PIK3CB is abnormally expressed in various carcinomas and affects the proliferation, invasion and drug resistance of cancer cells. However, its role in oesophageal squamous cell carcinoma (ESCC) is still unclear. In this study, PIK3CB was found to be highly expressed in ESCC tissues and cells and positively correlated with the poor prognosis of ESCC. Silencing PIK3CB inhibited the proliferation of ESCC cells, arrested the cell cycle, and promoted apoptosis. Mechanistic studies showed that the tumour-promoting effect of PIK3CB was achieved through PI3K/AKT/mTOR signalling pathway activation. Moreover, the high PIK3CB expression level in ESCC may be closely associated with the hypomethylation status of the gene promoter. In conclusion, PIK3CB promotes ESCC by activating the PI3K/AKT/mTOR signalling axis. PIK3CB may be a potential target in ESCC.

摘要

PIK3CB 在各种癌中异常表达,影响癌细胞的增殖、侵袭和耐药性。然而,其在食管鳞状细胞癌(ESCC)中的作用尚不清楚。本研究发现 PIK3CB 在 ESCC 组织和细胞中高表达,与 ESCC 的不良预后呈正相关。沉默 PIK3CB 抑制 ESCC 细胞的增殖,使细胞周期停滞,并促进细胞凋亡。机制研究表明,PIK3CB 通过激活 PI3K/AKT/mTOR 信号通路发挥促瘤作用。此外,ESCC 中 PIK3CB 的高表达水平可能与基因启动子的低甲基化状态密切相关。总之,PIK3CB 通过激活 PI3K/AKT/mTOR 信号轴促进 ESCC。PIK3CB 可能是 ESCC 的一个潜在靶点。

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