Chou Jinjiang, Wang Bingyu, Zheng Tianjing, Li Xiaoman, Zheng Lufeng, Hu Jinhang, Zhang Yan, Xing Yingying, Xi Tao
School of Life Science and Technology, China Pharmaceutical University, #24 Tongjiaxiang, Nanjing 210009, People's Republic of China; Jiangsu Key Laboratory of Carcinogenesis and Intervention, China Pharmaceutical University, #24 Tongjiaxiang, Nanjing 210009, People's Republic of China.
Jiangsu Key Laboratory of Carcinogenesis and Intervention, China Pharmaceutical University, #24 Tongjiaxiang, Nanjing 210009, People's Republic of China; Jingsu Key Laboratory for Pharmacology and Safety Evaluation of Chinese Materia Medica, School of Pharmacy, Nanjing University of Chinese Medicine, Nanjing 210023, People's Republic of China.
Biochem Biophys Res Commun. 2016 Mar 25;472(1):262-9. doi: 10.1016/j.bbrc.2016.02.102. Epub 2016 Feb 27.
Competitive endogenous messenger RNAs (ceRNAs) affect other RNAs transcription through competitively binding common microRNAs (miRNAs). In this study we identified long non-coding RNA (lncRNA) MALAT1 can function as a ceRNA of cell division cycle 42 (cdc42) 3'UTR in inducing migration and invasion of breast cancer cells via miR-1. We found that miR-1 bound both MALAT1 and cdc42 3'UTR directly. Further study showed that MALAT1 induced migration and invasion of breast cancer cells while reduced the level of cdc42. Our results suggest that MALAT1 regulated migration and invasion of breast cancer cells via affecting cdc42 through binding miR-1 competitively.
竞争性内源性信使核糖核酸（ceRNAs）通过竞争性结合共同的微小核糖核酸（miRNAs）来影响其他核糖核酸的转录。在本研究中，我们鉴定出长链非编码核糖核酸（lncRNA）MALAT1可作为细胞分裂周期蛋白42（cdc42）3'非翻译区的ceRNA，通过miR-1诱导乳腺癌细胞的迁移和侵袭。我们发现miR-1直接结合MALAT1和cdc42 3'非翻译区。进一步研究表明，MALAT1诱导乳腺癌细胞的迁移和侵袭，同时降低cdc42的水平。我们的结果表明，MALAT1通过竞争性结合miR-1影响cdc42，从而调节乳腺癌细胞的迁移和侵袭。
