microRNA-106b-mediated down-regulation of C1orf24 expression induces apoptosis and suppresses invasion of thyroid cancer.

摘要: // Gianna Carvalheira 1,* , Bruno Heidi Nozima and Janete Maria Cerutti 1 Genetic Bases of Thyroid Tumors Laboratory, Division Genetics, Department Morphology Universidade Federal de Sao Paulo, SP, Brazil * These authors have equally contributed to this work Correspondence to: Carvalheira, email: Keywords : C1orf24, NIBAN, FAM129A, miR-106b, follicular thyroid carcinoma papillary Received October 24, 2014 Accepted July 02, 2015 Published 22, Abstract We previously showed that C1orf24 expression is increased in carcinomas. Nonetheless, the mechanism underlying deregulation not fully understood. It has been widely demonstrated microRNAs are involved post-transcriptional gene regulation several diseases, including cancer. Using silico prediction approach, five bind 3’-untranslated region (3’-UTR) were identified. The two selected (miR-17-5p, miR-106b) tested 48 benign malignant lesions cell lines. miR-106b was down-regulated cancer specimens lines, while markedly increased. To demonstrate reduces expression, (WRO) (TPC1) lines transiently transfected with mimic. Ectopic mimic significantly inhibits mRNA protein both WRO TPC1 cells. Dual-luciferase report assays directly targets by binding its 3’-UTR. Moreover, miR-106b-mediated down-regulation apoptosis inhibited migration. additionally siRNA against decreased migration cycle progression induced apoptosis. In summary, our findings only provide new insights into molecular associated overexpression carcinomas but also show might increase proliferation Thus, decreasing levels, restoring function, may therapeutic implications.