Snail and Slug collaborate on EMT and tumor metastasis through miR-101-mediated EZH2 axis in oral tongue squamous cell carcinoma.

摘要: // Min Zheng 1, 2, * , Ya-ping Jiang Wei Chen 3, Kai-de Li 1 Xin Liu Shi-yu Gao Hao Feng Sha-sha Wang Jian Xiang-rui Ma Xiao Cen Ya-jie Tang 4 Yu Yun-feng Lin Ya-ling 5 Xin-hua Liang 6 State Key Laboratory of Oral Diseases West China Hospital Stomatology (Sichuan University), Chengdu Sichuan 610041, People's Republic 2 Department Stomatology, Zhoushan Hospital, Zhoushan, Zhejiang 316000, 3 and Maxillofacial Surgery, Tianjin Stomatological 300041, Fermentation Engineering (Ministry Education), Hubei University Technology, Wuhan 430068, Pathology, These authors have contributed equally to this work Correspondence to: Tang, e-mail: tangyaling@scu.edu.cn Liang, lxh88866@scu.edu.cn ; drliangxinhua@aliyun.com Keywords: tongue squamous cell carcinoma (OTSCC), Epithelial-mesenchymal transition (EMT), miR-101, Snail, Slug Received: November 03, 2014      Accepted: January 25, 2015      Published: February 09, 2015 ABSTRACT microRNAs(miRNAs) can regulate epithelial-mesenchymal (EMT) through transcription factors, however, little is known whether EMT factors modulate miRNAs further induce cancer metastasis. Here we show that overexpression Snail leads a mesenchymal phenotype morphology enhances invasion along with stem properties in oral (OTSCC) cells. Repression miR-101 expression by essential for Snail/Slug-induced malignant phenotypes. The suppression subsequently activates EZH2, the sole histone methyltransferase, inducing EMT, migration OTSCC Importantly, co-overexpression correlates poor survival elevated EZH2 two independent patient cohorts specimens. findings defined Slug/miR-101/EZH2 pathway as novel regulatory axis EMT-mediated-microRNA signaling.