Long non-coding RNA MALAT1 is up-regulated in ovarian cancer tissue and promotes SK-OV-3 cell proliferation and invasion.

Ovarian cancer is a gynecological malignancy worldwide. Long non-coding RNAs (lncRNAs) research is an emerging area in cancer studies, but little is known about lncRNA metastasis associated lung adenocarcinoma transcript 1 (MALAT1) in ovarian cancer. This study aims to investigate expression and roles of MALAT1 in ovarian cancer. MALAT1 level was detected in 20 ovarian cancer patients. MALAT1 expression was promoted by transforming growth factor β1 (TGFB1) treatment and inhibited by siRNA transfection in human ovarian cancer cell line SK-OV-3, after which changes in cell viability, proliferation, migration and invasion were analyzed by MTT, colony formation and Transwell assays. Protein levels of mitogen-activated protein kinase factors, including MAPK kinase 1 (MEK1), extracellular signal-regulated kinase (ERK1), p38 and c-Jun N-terminal kinase 1 (JNK1), were detected by western blot. Results showed that MALAT1 was significantly up-regulated in ovarian cancer tissues compared to adjacent normal tissues (P < 0.001), and its expression was correlated to tumor size (r2 = 0.7770, P < 0.0001) and metastasis. TGFB1 and siRNA successfully altered MALAT1 levels in SK-OV-3 cells. Knockdown of MALAT1 suppressed SK-OV-3 cell viability, proliferation, migration and invasion (P < 0.05), and inhibited phosphorylation of MEK1, ERK1, p38 and JNK1, which suggested that MALAT1 promoted ovarian cancer cell proliferation, migration and invasion, and that MAPK pathways might be one of the regulatory mechanisms of MALAT1. This study reveals that MALAT1 is a potential biomarker for tumor growth and metastasis, as well as a promising therapeutic target in ovarian cancer, facilitating further ovarian cancer research.