Effect of PI3K gene silencing on growth, migration and related proteins expression of CD40 signal-mediated gastric cancer cells

被引：5
|
作者：
Li, Rui [1 ]
Chen, Wei-Chang [1 ]
Pang, Xue-Qin [1 ]
Tian, Wen-Yan [1 ]
Wang, Wei-Peng [2 ]
Zhang, Xue Guang [3 ]
机构：
[1] Soochow Univ, Affiliated Hosp 1, Dept Gastroenterol, Key Lab Med & Clin Immunol Jiangsu Prov, Suzhou 215006, Peoples R China
[2] Soochow Univ, Coll Pharm, Suzhou 215007, Peoples R China
[3] Soochow Univ, Key Lab Med & Clin Immunol Jiangsu Prov, Inst Med Biotechnol, Suzhou 215007, Peoples R China
来源：
MOLECULAR BIOLOGY REPORTS | 2013年 / 40卷 / 02期
基金：
中国国家自然科学基金;
关键词：
PI3K siRNA; Gastric cancer; sCD40L; PI3K/Akt signal pathway; AGS; CARCINOMA-CELLS; HEPATOCELLULAR-CARCINOMA; COLORECTAL-CANCER; IN-VITRO; ANGIOGENESIS; APOPTOSIS; ACTIVATION; PATHWAY; TRANSCRIPTION; STIMULATION;
D O I：
10.1007/s11033-012-2141-7
中图分类号：
Q5 [生物化学]; Q7 [分子生物学];
学科分类号：
071010 ; 081704 ;
摘要：
In this study, we investigate effect of PI3K gene silencing on growth, migration and related proteins expression of CD40 signal-mediated gastric cancer cells. We observed that combination of sCD40L with PI3K siRNA could significantly inhibit AGS cells growth, block cells in G1 phase, and promote tumour cells apoptosis after 24 h treatment. Transwell test showed that numbers of cells per visual field in group PI3K siRNA or group sCD40L (after 24 h PI3K siRNA or sCD40L alone treatment) were fewer than that (32.54 +/- A 4.22) in control group. Numbers of cells per visual field in (after 24 h combination treatment of PI3K siRNA with sCD40L) were significantly fewer than that in group PI3K siRNA or group sCD40L. Compared with group sCD40L, expression level of Fas protein in group sCD40L + PI3K siRNA was significantly increased. The findings suggest that PI3K siRNA may strengthen CD40-induced specific antitumour effect via blocking PI3K/Akt signal pathway, resisting tumour immunoediting regulated by CD40 signal. Combination of sCD40L and PI3K siRNA is an important mechanism of gastric cancer therapy.
引用
收藏
页码：999 / 1008
页数：10
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