Abstract
Increasing evidence demonstrated that long non-coding RNA growth-arrest-specific transcript 5 (GAS5) serves as a critical regulator in cancer development and progression. However, its function and mechanism in nasopharyngeal carcinoma (NPC) is still not well elucidated. In this study, we investigate the functional role as well as the molecular mechanism of GAS5 in NPC progression. Our results indicated that GAS5 expression was elevated in NPC tissues and cells. High GAS5 expression was correlated with poor prognosis of NPC patients. GAS5 knockdown suppressed proliferation, migration and invasion, and induced apoptosis in NPC cells. Moreover, GAS5 could epigenetically suppress PTEN expression via recruiting enhancer of zeste homolog 2 (EZH2). PTEN knockdown could reverse the inhibitory effect of GAS5 inhibition on NPC progression. Furthermore, GAS5 knockdown suppressed the tumor growth in vivo. In summary, knockdown of GAS5 repressed proliferation, migration and invasion, and promoted apoptosis in NPC through epigenetically silencing PTEN via recruiting EZH2.