Abstract

BACKGROUND: It is well known that long noncoding RNA (lncRNA) metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) is closely correlated with the tumorigenesis of multiple cancers, including renal cell carcinoma (RCC). However, the potential functional mechanism is still elusive.

MATERIAL AND METHODS: In our present research, quantitative real-time polymerase chain reaction (qRT-PCR) was performed for the measurement of MALAT1 and miR-429. CCK-8 assay and Transwell assay were performed for the proliferation, migration, and invasion abilities of RCC cells. Dual-luciferase reporter assay was performed to validate the interaction within MALAT1 and miR-429.

RESULTS: Data found that MALAT1 was overexpressed in RCC clinical samples and cell lines. Moreover, loss-of-functional experiments showed that MALAT1 knockdown suppress the proliferation, migration, and invasion abilities of RCC cells. RT-PCR showed that miR-429 expression was downregulated in RCC cell lines, which was negatively correlated with that of MALAT1. Bioinformatics analysis suggested that miR-429 had complementary binding sequences with MALAT1, which was confirmed by dual-luciferase reporter assay.

CONCLUSIONS: In summary, our results concluded that MALAT1 functioned as an oncogene in RCC by sponging miR-429, acting as its competing endogenous RNA (ceRNA).

Keywords: Carcinoma, Renal Cell, Nephrology