LAUSR

OBJECTIVE This study was designed to investigate the specific mechanism underlying the regulatory effect of long noncoding ribonucleic acids (lncRNAs) MSTO2P on lung cancer (LCa) cell proliferation and autophagy via regulating enhancer of zeste homolog (EZH2) expression. PATIENTS AND METHODS Quantitative real-time polymerase chain reaction (qRT-PCR) was applied to analyze the levels of MSTO2P and EZH2 in 40 pairs of LCa tissues and corresponding adjacent tissues, as well as in LCa cell lines (H1299, H23, A549) and human bronchial epithelial cells (BEAS-2B). Besides, the effect of MSTO2P on cell proliferation ability was detected by cell counting kit-8 (CCK-8) and plate cloning experiments. The interaction between MTS02P and EZH2 as well as their effects on cell autophagy ability were examined by qRT-PCR and Western blot. RESULTS The qRT-PCR results showed that MSTO2P expression in LCa tissues was remarkably higher than that in adjacent tissues. Meanwhile, compared with human bronchial epithelial cells, the level of MSTO2P was remarkably up-regulated in LCa cells. After down-regulating MSTO2P, the cell proliferation ability was weakened, and the protein levels of autophagy-related genes including Agt5, LC-3I, and LC-3II were remarkably down-regulated. At the same time, EZH2 expression in LCa tissues was also remarkably up-regulated relative to adjacent tissues, and it was positively correlated with the expression of MSTO2P. In addition, after down-regulating MSTO2P, the EZH2 level was also remarkably reduced. Further experimental results revealed that EZH2 down-regulation could impair the cell proliferation ability and down-regulate the expressions of autophagy genes such as Agt5, LC-3I, and LC-3II. CONCLUSIONS LncRNA MSTO2P promotes LCa cell proliferation and autophagy by up-regulating EZH2. Therefore, MSTO2P may be a potential therapeutic target for LCa.