Research Papers:

BMX/Etk promotes cell proliferation and tumorigenicity of cervical cancer cells through PI3K/AKT/mTOR and STAT3 pathways

Yuanyuan Li, Nan Cui, Peng-Sheng Zheng and Wen-Ting Yang _

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Oncotarget. 2017; 8:49238-49252. https://doi.org/10.18632/oncotarget.17493

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Yuanyuan Li1, Nan Cui1, Peng-Sheng Zheng1,2 and Wen-Ting Yang1

1Department of Reproductive Medicine, First Affiliated Hospital of Xi’an Jiaotong University, Xi’an, People’s Republic of China

2Section of Cancer Stem Cell Research, Key Laboratory of Environment and Genes Related to Diseases, Ministry of Education of The People’s Republic of China, Xi’an, People’s Republic of China

Correspondence to:

Wen-Ting Yang, email: [email protected]

Peng-Sheng Zheng, email: [email protected]

Keywords: BMX, cell proliferation, cervical carcinoma, AKT, STAT3

Received: February 15, 2017     Accepted: April 17, 2017     Published: April 27, 2017


Bone marrow X-linked kinase (BMX, also known as Etk) has been reported to be involved in cell proliferation, differentiation, apoptosis, migration and invasion in several types of tumors, but its role in cervical carcinoma remains poorly understood. In this study, we showed that BMX expression exhibits a gradually increasing trend from normal cervical tissue to cervical cancer in situ and then to invasive cervical cancer tissue. Through BMX-IN-1, a potent and irreversible BMX kinase inhibitor, inhibited the expression of BMX, the cell proliferation was significantly decreased. Knockdown of BMX in HeLa and SiHa cervical cancer cell lines using two different silencing technologies, TALEN and shRNA, inhibited cell growth in vitro and suppressed xenograft tumor formation in vivo, whereas overexpression of BMX in the cell line C-33A significantly increased cell proliferation. Furthermore, a mechanism study showed that silencing BMX blocked cell cycle transit from G0/G1 to S or G2/M phase, and knockdown of BMX inhibited the expression of p-AKT and p-STAT3. These results suggested that BMX can promote cell proliferation through PI3K/AKT/mTOR and STAT3 signaling pathways in cervical cancer cells.

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