Lijuan Ke1, Yanping Chen1, Yiying Li2, Zheng Chen1, Yihui He3, Jiahua Liu1, Yingfeng Zhuang4. 1. Department of Gynecology, Shengli Clinical Medical College of Fujian Medical University and Fujian Provincial Hospital, No. 134 Dong Street, Fuzhou, Fujian 350001, People's Republic of China. 2. Department of Gynecology and Obstetrics, Shengli Clinical Medical College of Fujian Medical University and Fujian Provincial Hospital South Branch, No. 516 Jinrong South Street, Fuzhou, Fujian 350028, People's Republic of China. 3. Department of Pathology, Shengli Clinical Medical College of Fujian Medical University and Fujian Provincial Hospital, No. 134 Dong Street, Fuzhou, Fujian 350001, People's Republic of China. 4. Department of Critical Care Medicine, Shengli Clinical Medical College of Fujian Medical University and Fujian Provincial Hospital South Branch, No. 516 Jinrong South Street, Fuzhou, Fujian 350028, People's Republic of China.
Abstract
BACKGROUND: Previous work has shown that miR-142-5p in cervical cancer tissues increased significantly compared with adjacent normal tissues. However, the function and the mechanism of miR-142-5p in cervical cancer have not been reported. METHODS: Quantitative reverse transcription-polymerase chain reaction (qRT-PCR) was used to determine the gene expression levels. MTT, flow cytometry, and transwell assays were performed to explore the functions of miR-142-5p in HeLa cells. The potential target gene of miR-142-5p was investigated via luciferase reporter assays. The protein expression levels were analyzed by Western blotting. RESULTS: We found that miR-142-5p expression was elevated but LIM homeobox transcription factor 1 alpha (LMX1A) was decreased in cervical cancer tissues and cells. Overexpression of miR-142-5p or knockdown of LMX1A inhibited cell apoptosis, promoted cell proliferation, migration, invasion abilities, and activated the Wnt/β-catenin pathway. However, knockdown of miR-142-5p or overexpression of LMX1A showed opposite results. LMX1A was identified as a direct target of miR-142-5p by luciferase reporter assays. Finally, rescue experiments demonstrated that LMX1A overexpression attenuated the carcinogenic effect of miR-142-5p mimic on HeLa cells. CONCLUSIONS: These findings suggested that miR-142-5p might be a cervical cancer oncogene and could serve as a potential therapeutic target for the treatment of cervical cancer.
BACKGROUND: Previous work has shown that miR-142-5p in cervical cancer tissues increased significantly compared with adjacent normal tissues. However, the function and the mechanism of miR-142-5p in cervical cancer have not been reported. METHODS: Quantitative reverse transcription-polymerase chain reaction (qRT-PCR) was used to determine the gene expression levels. MTT, flow cytometry, and transwell assays were performed to explore the functions of miR-142-5p in HeLa cells. The potential target gene of miR-142-5p was investigated via luciferase reporter assays. The protein expression levels were analyzed by Western blotting. RESULTS: We found that miR-142-5p expression was elevated but LIM homeobox transcription factor 1 alpha (LMX1A) was decreased in cervical cancer tissues and cells. Overexpression of miR-142-5p or knockdown of LMX1A inhibited cell apoptosis, promoted cell proliferation, migration, invasion abilities, and activated the Wnt/β-catenin pathway. However, knockdown of miR-142-5p or overexpression of LMX1A showed opposite results. LMX1A was identified as a direct target of miR-142-5p by luciferase reporter assays. Finally, rescue experiments demonstrated that LMX1A overexpression attenuated the carcinogenic effect of miR-142-5p mimic on HeLa cells. CONCLUSIONS: These findings suggested that miR-142-5p might be a cervical cancer oncogene and could serve as a potential therapeutic target for the treatment of cervical cancer.
Authors: Victor V Chizhikov; Anne G Lindgren; Yuriko Mishima; Richard W Roberts; Kimberly A Aldinger; George R Miesegaes; D Spencer Currle; Edwin S Monuki; Kathleen J Millen Journal: Proc Natl Acad Sci U S A Date: 2010-05-24 Impact factor: 11.205