Abstract:
:Dysregulation of microRNAs (miRNAs) occurs frequently in cervical carcinogenesis. miRNAs function as tumor-suppressors or oncogenes and are involved in tumor behavior. However, the expression and function of miR-27b in cervical carcinogenesis remain unknown. In the present study, we observed that miR-27b was significantly increased in cervical cancer cells and tissues, and upregulation of miR-27b was negatively associated with its direct target, cadherin 11 (CDH11). Upregulation of miR-27b significantly accelerated the proliferation, cell cycle transition from G1 to S phase, migration and invasion of C33A cells, while downregulation of miR-27b suppressed the proliferation and invasion of HeLa cells. Moreover, CDH11 cDNA transfection impaired the oncogenic effect of miR-27b on cancer cells. Knockdown of CDH11 attenuated the suppressive effect of an miR-27b inhibitor on cervical cancer cells. In addition, we found that CDH11 was involved in miR-27b-induced epithelial-mesenchymal transition (EMT) by regulating expression of E-cadherin, vimentin and N-cadherin. Our results for the first time indicate that miR-27b acting as an oncogene may play an important role in the progression of cervical cancer by modulating CDH11 and EMT.
journal_name
Oncol Repjournal_title
Oncology reportsauthors
Yao J,Deng B,Zheng L,Dou L,Guo Y,Guo Kdoi
10.3892/or.2015.4500subject
Has Abstractpub_date
2016-03-01 00:00:00pages
1645-51issue
3eissn
1021-335Xissn
1791-2431journal_volume
35pub_type
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