Abstract

BACKGROUND: The aim of this study was to clarify the potential function of LINC00922 in regulating the progression of lung cancer and its underling mechanism.

MATERIAL AND METHODS: Relative levels of LINC00922 in lung cancer tissues and cell lines was determined by quantitative polymerase chain reaction. Correlation between LINC00922 levels and pathological indexes of lung cancer patients was analyzed through the chi-square test. Subsequently, regulatory effects of LINC00922 on the proliferative, migratory, and invasive capacities of PC9 and A549 cells were evaluated. Western blot was conducted to determine the role of LINC00922 in mediating protein levels of CXCR4, E-cadherin, and vimentin. Through dual-luciferase reporter gene assay and functional experiments, the potential function of LINC00922/miRNA-204/CXCR4 regulatory loop in mediating the progression of lung cancer was explored.

RESULTS: LINC00922 was highly expressed in lung cancer and correlated to the poor prognosis of lung cancer patients. Overexpression of LINC00922 accelerated PC9 and A549 cells to proliferate, migrate, and invade. CXCR4 was upregulated in lung cancer tissues and cells, which promoted lung cancer cells to migrate and invade. LINC00922 regulated the level of CXCR4 and directly bound to miRNA-204/CXCR4. LINC00922 mediated the cellular behaviors of lung cancer cells via targeting the miRNA-204/CXCR4 axis.

CONCLUSIONS: LINC00922 was upregulated in lung cancer, and accelerated lung cancer cells to proliferate, migrate, and invade via targeting the miRNA-204/CXCR4 axis.

Keywords: Receptors, CXCR4, RNA, Long Noncoding, A549 cells, Aged, Cadherins, Databases, Genetic, Gene Expression Regulation, Neoplastic, Middle Aged, Neoplasm Invasiveness, Vimentin