Oncotarget

Research Papers:

Hypoxia induced Bcl-2/Twist1 complex promotes tumor cell invasion in oral squamous cell carcinoma

Yuansheng Duan, Qinghua He, Kai Yue, Haishan Si, Jiaxin Wang, Xuan Zhou and Xudong Wang _

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Oncotarget. 2017; 8:7729-7739. https://doi.org/10.18632/oncotarget.13890

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Abstract

Yuansheng Duan1,2,*, Qinghua He1,2,*, Kai Yue1,2,*, Haishan Si1,2, Jiaxin Wang1,2, Xuan Zhou1,2, Xudong Wang1,2

1Department of Maxillofacial and E.N.T Oncology, Tianjin Medical University Cancer Institute and Hospital, Tianjin 300060, China

2National Clinical Research Center for Cancer, Key Laboratory of Cancer Preventionand Therapy, Tianjin 300060, China

*These authors contributed equally to this work

Correspondence to:

Xudong Wang, email: [email protected]

Keywords: Bcl-2, Twist1, tumor invasion, EMT, oral squamous cell carcinoma

Received: February 18, 2016     Accepted: December 05, 2016     Published: December 10, 2016

ABSTRACT

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.


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