miR-216b suppresses tumor growth and invasion by targeting KRAS in nasopharyngeal carcinoma

• DOI: 10.1242/jcs.085050
• Publication Date: 2011-08-30T16:48:29Z
• Authors: Min Deng; Hailin Tang; Yanhong Zhou; Ming Zhou; Wei Xiong; Ying Zheng; Qiurong Ye; Xi Zeng; Qianjin Liao; Xiaofang Guo; Xiaoling Li; Jian Ma; Guiyuan Li
• Keywords: Male; 0301 basic medicine; Mice, Inbred BALB C; Nasopharyngeal Carcinoma; MAP Kinase Signaling System; Carcinoma; Down-Regulation; Mice, Nude; Nasopharyngeal Neoplasms; Cell Growth Processes; Immunohistochemistry; 3. Good health; Gene Expression Regulation, Neoplastic; Mice; MicroRNAs; 03 medical and health sciences; Genes, ras; Cell Line, Tumor; Gene Knockdown Techniques; Animals; Humans; Extracellular Signal-Regulated MAP Kinases; 3' Untranslated Regions

MicroRNAs (miRNAs) are small noncoding RNAs that are involved in various diseases, including cancer. In the present study, we found that miR-216b was downregulated in nasopharyngeal carcinoma (NPC) cell lines and specimens. Decreased expression of miR-216b was directly related to advanced clinical stage and lymph node metastasis. miR-216b levels correlated inversely with levels of KRAS protein during nasopharyngeal tumorigenesis. Furthermore, we demonstrated that miR-216b can bind to the 3′ untranslated region (UTR) of KRAS and inhibit expression of the KRAS protein. Both in vitro and in vivo assays revealed that miR-216b attenuated NPC cell proliferation, invasion and tumor growth in nude mice. miR-216b exerts its tumor suppressor function through inhibition of the KRAS-related AKT and ERK pathways. Our findings provide, for the first time, significant clues regarding the role of miR-216b as a tumor suppressor by targeting KRAS in NPC.