Hypoxia induced Bcl-2/Twist1 complex promotes tumor cell invasion in oral squamous cell carcinoma.
Hypoxia induced Bcl-2/Twist1 complex promotes tumor cell invasion in oral squamous cell carcinoma.
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DOI：
10.18632/oncotarget.13890
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发表时间：
2017-01-31
期刊：
影响因子：
--
通讯作者：
Wang X
中科院分区：
文献类型：
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作者：
Duan Y;He Q;Yue K;Si H;Wang J;Zhou X;Wang X
Bcl-2和Twist1可在肝细胞癌中被缺氧共同激活，促进肿瘤细胞转移和血管生成模拟，但它们在口腔鳞状细胞癌（OSCC）中的功能尚不清楚。我们采用了一组82例OSCC样本，通过免疫组化检测了Bcl-2和Twist1的共表达，并通过共免疫沉淀证实了Bcl-2和Twist1之间的相互作用。Bcl-2和Twist1过表达与较差的病理分级和肿瘤预后相关，两者是一个复合物。下调Bcl-2/Twist1可抑制细胞迁移，降低细胞侵袭，逆转细胞上皮-间质转化（EMT）过程。利用来自Tca8113细胞系的动物模型进一步验证了Bcl-2/Twist1缺失在抑制肿瘤EMT和生长中的作用。综上所述，Bcl-2/Twist1复合体可作为OSCC的潜在治疗靶点。
Bcl-2 and Twist1 can be coactivated by hypoxia in hepatocellular carcinoma to promote tumor cell metastasis and vasculogenic mimicry, but their function in oral squamous cell carcinoma (OSCC) remains undefined. We employed a cohort of 82 cases of OSCC samples to examine the coexpression of Bcl-2 and Twist1 by immunohistochemistry and demonstrate the interaction between Bcl-2 and Twist1 by coimmunoprecipitation. Bcl-2 and Twist1 overexpression was associated with a poor pathological grade and tumor prognosis, and the two factors functions as a complex. Knocking down Bcl-2/Twist1 inhibited cell migration, decreased cell invasion and inversed cell epithelial-mesenchymal transition (EMT) procession. An animal model derived from the Tca8113 cell line was used to further validate the role of Bcl-2/Twist1 depletion in suppressing tumor EMT and growth. In conclusion, Bcl-2/Twist1 complex can be treated as a potential therapeutic target for OSCC.