RETRACTED ARTICLE: Impairment of growth of gastric carcinoma by miR-133-mediated Her-2 inhibition

• Published in: Tumor biology Vol. 36; no. 11; pp. 8925 - 8930
• Main Authors: Zhang, Xiao-Tao, Zhang, Zhen, Xin, Yong-Ning, Ma, Xue-Zhen, Xuan, Shi-Ying
• Format: Journal Article
• Language: English
• Published: Dordrecht Springer Netherlands 01.11.2015
• Subjects: Biomedical and Life Sciences; Biomedicine; Cancer Research; Research Article; Her-2; Gastric carcinoma (GC); MicroRNAs (miRNA); Growth; MiR-133; Apoptosis
• ISSN: 1010-4283; 1423-0380
• DOI: 10.1007/s13277-015-3637-2

Gastric carcinoma (GC) is a leading cause of cancer-related death in China. Dysregulation of microRNAs (miRNAs) has been shown to contribute to the development of GC, whereas the role of miR-133 in GC is unknown. Here, we analyzed the levels of miR-133 in GC tissues by reverse and quantitative transcription polymerase chain reaction (RT-qPCR). We overexpressed or inhibited miR-133 in GC cells. Cell growth was analyzed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, and cell apoptosis was evaluated by fluorescence-activated cell sorting (FACS) analysis. Targeted genes were predicted by a bioinformatics algorithm and confirmed by a dual-luciferase reporter assay. We detected lower miR-133 levels in GC tissues compared with normal gastric tissue. Moreover, the low miR-133 levels were correlated with low survival rate. Overexpression of miR-133 inhibited cell growth and promoted apoptosis, while depletion of miR-133 increased cell growth and suppressed apoptosis. Moreover, the 3′-untranslated region (3′UTR) of Her-2, the epidermal growth factor receptor (EGFR) that transduces cell growth signals, appeared to be targeted by miR-133. Together, these data suggest that reduced miR-133 levels in GC tissues promote GC growth, which possibly contributes to a low survival rate of GC patients. MiR-133 may target Her-2 to suppress GC cell growth.