B7-H3 inhibits apoptosis of gastric cancer cell by interacting with Fibronectin

被引:11
|
作者
Sun, Meiyun [1 ,2 ]
Xie, Jinjing [1 ,2 ]
Zhang, Dongze [1 ,2 ]
Chen, Chunyang [1 ,2 ]
Lin, Simin [1 ,2 ]
Chen, Yan [2 ]
Zhang, Guangbo [1 ,2 ]
机构
[1] Soochow Univ, Med Coll, 199 Ren Ai Rd, Suzhou 215100, Jiangsu, Peoples R China
[2] Soochow Univ, Affiliated Hosp 1, Jiangsu Inst Clin Immunol, 708 Ren Min Rd, Suzhou 215100, Jiangsu, Peoples R China
来源
JOURNAL OF CANCER | 2021年 / 12卷 / 24期
基金
中国国家自然科学基金;
关键词
Gastric cancer; B7-H3; Fibronectin; adhesion; apoptosis; BREAST-CANCER; CYCLE ARREST; ACTIVATION; EXPRESSION; MOLECULE; OVEREXPRESSION; MITOCHONDRIA; RESISTANCE; CARCINOMA; PATHWAY;
D O I
10.7150/jca.59263
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Anti-apoptosis has been widely accepted as a hallmark of malignancy. B7-H3, a type I transmembrane protein, plays a key role in anti-apoptosis and immune escape, but its regulation during cancer development remains unclear. To investigate how the effect of anti-apoptosis is regulated by B7-H3 in gastric cancer, we stably knocked down B7-H3 gene by shRNA in MGC-803 and MKN-45 cells. The correlation between B7-H3 and Fibronectin (FN) expression were investigated by bioinformatics in public data from TCGA (The Cancer Genome Atlas). Here, we reported that B7-H3 expression is positively correlated with FN in clinical gastric cancer samples, and B7-H3 promoted adhesion and inhibited apoptosis of gastric cancer cell through an FN-dependent pathway. Mechanistically, B7-H3 interacted with FN and subsequently activated PI3K/AKT signaling pathway, a critical mediator of oncogenic signaling. In addition, exogenous FN could inhibit the expression of pro-apoptosis-related proteins such as Caspase 3, Caspase 8, Caspase 9, Box , p53, Apaf-1 and Cleaved PARP, and upregulated the levels of signal molecule p-PI3K, p-AKT and anti-apoptotic proteins Bcl-2 in B7-H3(h)(igh) group, as compared with those in B7-H3(low) group. In conclusion, we here for the first time revealed that B7-H3 inhibits apoptosis of gastric cancer cell through regulation of FN-mediated PI3K/AKT signaling pathways.
引用
收藏
页码:7518 / 7526
页数:9
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