MicroRNA-216b is Down-Regulated in Human Gastric Adenocarcinoma and Inhibits Proliferation and Cell Cycle Progression by Targeting Oncogene HDAC8

We reported a significantly decreased expression of miR-216b in GC clinical specimens compared with paired non-cancerous tissues. We also observed a significant down-regulation of miR-216b expression in GC cell lines AGS and GC9811 (p < 0.0001). The introduction of miR-216b suppressed GC cell proliferation and cell cycle progression by targeting HDAC8, an oncogene shown to promote malignant tumor development with a potential miR-216b binding site in its 3′ untranslated region. HDAC8 expression was shown to be significantly increased in AGS and GC9811 cell lines (p < 0.0001) and GC tissues compared with controls. Moreover, HDAC8 inhibition suppressed cell cycle progression compared with control groups (22 % ± 1.6 % vs 34 % ± 2.1), indicating that HDAC8 may function as an oncogene in the development of GC. Furthermore, HDAC8 expression was negatively correlated (p < 0.0001), while miR-216b expression was positively correlated with the clinical outcome of GC patients (p < 0.0001). Discussion Our data suggest that miR-216b functions as a tumor suppressor in human GC by, at least partially, targeting HDAC8.
Source: Targeted Oncology - Category: Cancer & Oncology Source Type: research