LncRNA GAS5 suppresses proliferation, migration, invasion, and epithelial mesenchymal transition in oral squamous cell carcinoma by regulating the miR 21/PTEN axis
Abstract Growth arrest specific transcript 5 (GAS5) functions as a tumor suppressor in a variety of cancers. GAS5 has been reported to be down regulated in oral squamous cell carcinoma (OSCC) The aim of this study was to investigate the mechanisms of how GAS5 acts as a tumor suppressor in OSCC. qRT PCR, cell viability, wound healing, and transwell assays showed that knockdown of GAS5 increased miR 21 expression and promoted proliferation, migration, invasion, and epithelial mesenchymal transition of OSCC cells. In contrast, overexpression of GAS5 showed the opposite effects. Furthermore, miR 21 overexpression reversed the effect of GAS5. Western blot showed that knockdown of GAS5 suppressed PTEN, while phosphorylation of Akt was promoted. PCNA, cyclinD1, and Ki 67 were up regulated, indicating enhanced proliferation. E cadherin was down regulated, while N cadherin, vimentin, and snail1 were increased, indicating augmented epithelial mesenchymal transition. Overexpression of GAS5 regulated these proteins inversely. Overexpression of miR 21 reversed the effect of GAS5 on these proteins. Taken together, GAS5 suppresses proliferation, migration, invasion, and epithelial mesenchymal transition in OSCC through the miR 21/PTEN axis and might be a novel therapeutic target for OSCC.
Experimental cell research