Oncotarget

Research Papers:

Chemotherapy-mediated miR-29b expression inhibits the invasion and angiogenesis of cervical cancer

Yunyun Li, Zhongzu Zhang, Zhenghua Xiao, Ying Lin, Tangshu Luo, Qin Zhou and Xiaojing Zhang _

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Oncotarget. 2017; 8:14655-14665. https://doi.org/10.18632/oncotarget.14738

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Abstract

Yunyun Li1,*, Zhongzu Zhang2,*, Zhenghua Xiao1, Ying Lin1, Tangshu Luo1, Qin Zhou3, Xiaojing Zhang1

1Department of Gynecology and Obstetrics, The Yongchuan Hospital of Chongqing Medical University, Chongqing 402160, PR China

2Department of Orthopedics, The Yongchuan Hospital of Chongqing Medical University, Chongqing 402160, PR China

3Department of Gynecology and Obstetrics, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, PR China

*These authors contributes to this work

Correspondence to:

Qin Zhou, email: [email protected]

Xiaojing Zhang, email: [email protected]

Keywords: cervical cancer, miR-29b, STAT3, chemotherapy, EMT

Received: November 14, 2016     Accepted: January 11, 2017     Published: January 19, 2017

ABSTRACT

Radiotherapy combined with platinum-based chemotherapy is the standard-of-care of locally advanced cervical cancer (CC) patients, while nearly 50% of patients do not respond to standard chemotherapy. Thus, identification of relative molecules participated in chemotherapy might provide new insights in the treatment of CC. In this study, we found a cohort of miRNAs were dysregulated upon treatment with cisplatin, among of which miR-29b was the most upregulated one. We further detected its expression in CC tissues, and found that miR-29b was significantly suppressed in CC and its precancerous lesions, HSIL tissues, and was negatively related with tumor invasion. However, upon treatment with cisplatin, the expression of miR-29b was significantly up-regulated. The biological function assays showed that overexpression of miR-29b suppressed the invasion, EMT procedure and angiogenesis of cervical cancer cells in vitro and inhibited tumor growth and neovascularization in vivo through targeting STAT3 signal pathway. While, inhibition of miR-29b could prevent the cisplatin-induced epithelial features, cell movement and angiogenesis of CC cells, which means miR-29b/STAT3 axis participates in the chemotherapy of cisplatin in CC. Collectively, our data suggest that chemotherapy-mediated miR-29b expression participates in the initiation and progression of cervical cancer through suppressing the proliferation, EMT procedure and angiogenesis of cervical cancer cells by targeting STAT3 signal pathway.


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