MicroRNA-140-5p targets insulin like growth factor 2 mRNA binding protein 1 (IGF2BP1) to suppress cervical cancer growth and metastasis

// Yanlin Su 1 , Jie Xiong 2 , Jinyue Hu 3 , Xin Wei 1 , Xuelian Zhang 1 , Lijuan Rao 1 1 Department of Obstetrics and Gynecology, Changsha Central Hospital, Changsha, China 2 Department of Epidemiology and Health Statistcs, XiangYa School of Public Health, Central South University, Changsha, China 3 Medical Research Center, Changsha Central Hospital, Changsha, China Correspondence to: Lijuan Rao, email: raolijuan@126.com Xuelian Zhang, email: xlianz@126.com 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.