Zhiming Wu1, Huangen Wang2, Sunyang Fang2, Chaoyang Xu3. 1. Department of Surgery, Shaoxing Hospital of China Medical University, 1 Huayu Road, Shaoxing 312030, China. Electronic address: xucy15@163.com. 2. Department of Surgery, Shaoxing Hospital of China Medical University, 1 Huayu Road, Shaoxing 312030, China. 3. Department of Breast and Thyroid Surgery, Shaoxing People's Hospital, 568 Zhongxingbei Road, Shaoxing 312000, China.
Abstract
AIMS: Gastric carcinoma (GC) is among the leading causes of cancer-related deaths in China. Growing evidence indicates that dysregulation of miRNAs contributes to GC development. Although it has been shown that miR-449c acts as a tumor suppressor in lung cancer, the role of miR-449c in GC remains unclear. MAIN METHODS: Here, we analyzed miR-449c levels in GC tissues and cell lines by RT-qPCR. We also overexpressed and inhibited miR-449c by transfecting miRNA mimics and antisense oligonucleotides (ASO), respectively. Cell growth was analyzed by MTT assay, and cell apoptosis was evaluated by FACS analysis. MiR-449c target genes were predicted using bioinformatics algorithms and confirmed by a dual luciferase reporter assay. KEY FINDINGS: We detected lower miR-449c levels in GC tissues; the low miR-449c levels correlated with low survival rate. Overexpression of miR-449c inhibited cell growth and promoted apoptosis, while depletion of miR-449c increased cell growth and suppressed apoptosis. Moreover, the 3' UTR of MET, an oncogene that activates tumor cell growth, appeared to be targeted by miR-449c. SIGNIFICANCE: Together, we showed that the reduced miR-449c levels in GC tissues promote GC growth, which possibly contributes to the low survival rate of GC patients. Mechanistically, miR-449c may target MET to suppress GC cell growth.
AIMS: Gastric carcinoma (GC) is among the leading causes of cancer-related deaths in China. Growing evidence indicates that dysregulation of miRNAs contributes to GC development. Although it has been shown that miR-449c acts as a tumor suppressor in lung cancer, the role of miR-449c in GC remains unclear. MAIN METHODS: Here, we analyzed miR-449c levels in GC tissues and cell lines by RT-qPCR. We also overexpressed and inhibited miR-449c by transfecting miRNA mimics and antisense oligonucleotides (ASO), respectively. Cell growth was analyzed by MTT assay, and cell apoptosis was evaluated by FACS analysis. MiR-449c target genes were predicted using bioinformatics algorithms and confirmed by a dual luciferase reporter assay. KEY FINDINGS: We detected lower miR-449c levels in GC tissues; the low miR-449c levels correlated with low survival rate. Overexpression of miR-449c inhibited cell growth and promoted apoptosis, while depletion of miR-449c increased cell growth and suppressed apoptosis. Moreover, the 3' UTR of MET, an oncogene that activates tumor cell growth, appeared to be targeted by miR-449c. SIGNIFICANCE: Together, we showed that the reduced miR-449c levels in GC tissues promote GC growth, which possibly contributes to the low survival rate of GC patients. Mechanistically, miR-449c may target MET to suppress GC cell growth.
Authors: Fan Wang; Juan Lu; Xiaohong Peng; Jie Wang; Xiong Liu; Xiaomei Chen; Yiqi Jiang; Xiangping Li; Bao Zhang Journal: J Exp Clin Cancer Res Date: 2016-01-22