Research Papers:
MicroRNA-140-5p targets insulin like growth factor 2 mRNA binding protein 1 (IGF2BP1) to suppress cervical cancer growth and metastasis
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Abstract
Yanlin Su1, Jie Xiong2, Jinyue Hu3, Xin Wei1, Xuelian Zhang1, Lijuan Rao1
1Department of Obstetrics and Gynecology, Changsha Central Hospital, Changsha, China
2Department of Epidemiology and Health Statistcs, XiangYa School of Public Health, Central South University, Changsha, China
3Medical Research Center, Changsha Central Hospital, Changsha, China
Correspondence to:
Lijuan Rao, email: [email protected]
Xuelian Zhang, email: [email protected]
Keywords: cervical cancer, microRNA-140-5p, IGF2BP1, tumor suppressor
Received: January 05, 2016 Accepted: August 22, 2016 Published: August 31, 2016
ABSTRACT
MicroRNAs (miRNAs) are a class of small non-coding RNA molecules that play important roles in carcinogenesis and tumor progression. Previous studies have revealed that MicroRNA-140-5p (miR-140-5p) was abnormally expressed in several cancers. However, its function and possible mechanism in cervical cancer (CC) remains unknown. In this study, the data mining results showed that miR-140-5p was down-regulated in CC specimens and the down-regulation of miR-140-5p was associated with CC poor prognosis. These observations prompted us to further investigate the roles and mechanisms of miR-140-5p in human CC pathogenesis. We found that the over-expression/inhibition of miR-140-5p significantly decreased/increased cell proliferation, migration, and invasion in CC cells in vitro. Meanwhile, the results from in vivo assays showed that the over-expression of miR-140-5p induced significantly suppression of tumor growth and metastasis in nude mice. Furthermore, Insulin like growth factor 2 mRNA binding protein 1 (IGF2BP1) was identified as a direct target of miR-140-5p, and both gain-of-function and loss-of-function assays revealed that IGF2BP1 is also a functional target of miR-140-5p. Taken together, our findings suggested a novel miR-140-5p-IGF2BP1 regulatory circuit for CC pathogenesis, and miR-140-5p may be a potential target for CC therapy.
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