Research Papers:
MiR-142 inhibits the development of cervical cancer by targeting HMGB1
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Abstract
Daqiong Jiang1,*, Huiyan Wang2,*, Zhuyan Li1, Zhen Li1, Xin Chen1, Hongbing Cai1
1Department of Gynecological Oncology, Zhongnan Hospital of Wuhan University, Hubei Key Laboratory of Tumor Biological Behaviors, Hubei Cancer Clinical Study Center, Wuhan 430071, Hubei, P.R. China
2Department of Gynecological Oncology, Hospital of Wuhan University of Technology, Wuhan 430070, Hubei, P.R. China
*These authors contributed equally to this work and co-first authors
Correspondence to:
Hongbing Cai, email: [email protected]
Keywords: miR-142, HMGB1, cervical cancer
Received: October 11, 2016 Accepted: October 28, 2016 Published: November 05, 2016
ABSTRACT
It has been reported that miRNAs is deregulated in diverse human cancers, involving human cervical cancer. However, the clinical significances and potential mechanisms of miR-142 in the development and progression of cervical cancer were not elucidated completely till now. In this study, we found that the expression of miR- 142 was obviously down-regulated in human cervical cancer tissues and a panel of cell lines. According to statistics, the expression of miR-142 was negatively related to advanced FIGO stage and lymphatic metastasis (p < 0.001). Furthermore, our functional analysis revealed the overexpression of miR-142 affected cell proliferation and invasiveness, and enhanced cell apoptosis in representative SiHa and HeLa cells. Based on the molecular level, our findings showed the 3' untranslated region (3’-UTR) of high-mobility group box 1 protein (HMGB1) was a direct target of miR-142, and determined an inverse correlation with the expression of miR-142. Ectopic expression of HMGB1 could attenuate the inhibitory impact of miR-142 on the proliferation and invasiveness of cervical cancer cells. In conclusion, the present work suggested that miR-142 affects cervical cancer cell proliferation and invasiveness, and enhances cell apoptosis via directly targeting the expression of HMGB1, and these findings may lay a novel foundation for the promising therapy target of cervical cancer.

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