J Ke1, B-H Zhang, Y-Y Li, M Zhong, W Ma, H Xue, Y-D Wen, Y-D Cai. 1. Department of Gastroenterology, Xiyuan Hospital, China Academy of Chinese Medical Sciences, Beijing, China. doctor_cyd@163.com.
Abstract
OBJECTIVE: MiR-1 has been reported to act as an inhibitory microRNA in gastric cancer (GC). This study aimed to investigate the regulatory mechanism by which miR-1-3p blocks the progression of GC by targeting stanniocalcin 2 (STC2). PATIENTS AND METHODS: The expression level of miR-1-3p in GC was assessed via quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). Expressions of STC2 were measured by qRT-PCR and Western blot analysis. Proliferation and invasion assays were detected by MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide) and transwell assays, respectively. Moreover, the dual-luciferase reporter assay was used to confirm the binding sites between miR-1-3p and STC2. RESULTS: MiR-1-3p was significantly down-regulated in GC. Moreover, abnormal expression of miR-1-3p was correlated with GC tumor size. Functionally, overexpression of miR-1-3p inhibited proliferation and invasion in GC by inhibiting stanniocalcin 2 (STC2) expressions. In contrast, STC2 was significantly up-regulated in GC. Furthermore, miR-1-3p negatively regulated STC2 expression in GC. The upregulation of STC2 weakened the inhibitory effect of miR-1-3p in GC. CONCLUSIONS: MiR-1-3p suppressed cell proliferation and invasion by targeting STC2 in GC, providing a novel therapeutic target for GC.
OBJECTIVE:MiR-1 has been reported to act as an inhibitory microRNA in gastric cancer (GC). This study aimed to investigate the regulatory mechanism by which miR-1-3p blocks the progression of GC by targeting stanniocalcin 2 (STC2). PATIENTS AND METHODS: The expression level of miR-1-3p in GC was assessed via quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). Expressions of STC2 were measured by qRT-PCR and Western blot analysis. Proliferation and invasion assays were detected by MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide) and transwell assays, respectively. Moreover, the dual-luciferase reporter assay was used to confirm the binding sites between miR-1-3p and STC2. RESULTS: MiR-1-3p was significantly down-regulated in GC. Moreover, abnormal expression of miR-1-3p was correlated with GCtumor size. Functionally, overexpression of miR-1-3p inhibited proliferation and invasion in GC by inhibiting stanniocalcin 2 (STC2) expressions. In contrast, STC2 was significantly up-regulated in GC. Furthermore, miR-1-3p negatively regulated STC2 expression in GC. The upregulation of STC2 weakened the inhibitory effect of miR-1-3p in GC. CONCLUSIONS: MiR-1-3p suppressed cell proliferation and invasion by targeting STC2 in GC, providing a novel therapeutic target for GC.