Long Non-Coding RNA (lncRNA) Metastasis-Associated Lung Adenocarcinoma Transcript 1 (MALAT1) Promotes Cell Proliferation and Migration by Regulating miR-143-3p and MAGE Family Member A9 (MAGEA9) in Oral Squamous Cell Carcinoma

BACKGROUND: lncRNA MALAT1 is one of the most widely studied lncRNAs associated with various human cancers. The present study explored the functions and potential regulatory mechanisms of MALAT1 in oral squamous cell carcinoma (OSCC). MATERIAL/METHODS: We assessed levels of MALAT1, miR-143-3p, and MAGEA9 expression in OSCC tissues and cell lines by quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot assay. Proliferation and migration of CAL-27 cells were detected via CCK-8 and transwell assays, respectively. To study the relationships among MALAT1, miR-143-3p, and MAGEA9, we performed dual-luciferase assay and assessed the results using Spearman correlation analysis. RESULTS: QRT-PCR results showed that MALAT1 and MAGEA9 were expressed at higher levels and miR-143-3p was expressed at lower levels in OSCC tissues. Dramatic suppression of cell proliferation and migration abilities were caused by MALAT1 knockdown or miR-143-3p overexpression in CAL-27 cells. MALAT1 directly interacted with and negatively regulated miR-143-3p. Moreover, MAGEA9 was validated as a miR-143-3p target gene and was found to be negatively regulated by it. MALAT1 knockdown suppressed MAGEA9 protein expression and had the same effect as MAGEA9 knockdown. Additionally, MAGEA9 knockdown inhibited CAL-27 cell proliferation and migration abilities. Finally, in OSCC tissues, MALAT1 and miR-143-3p expression were negatively correlated and MALAT1 was positively correlated with MAGEA9 expression, while an inverse correlation between MAGEA9 and miR-143-3p expression was observed. CONCLUSIONS: Taken together, our results suggest that MALAT1 functions as a competing endogenous RNA (ceRNA) in promoting OSCC cell proliferation and migration abilities through the miR-143-3p/MAGEA9 axis, thus providing new therapeutic targets for treatment of OSCC.