Long non-coding RNA MALAT1 correlates with cell viability and mobility by targeting miR-22-3p in renal cell carcinoma via the PI3K/Akt pathway

Abstract

Renal cell carcinoma (RCC) is one of the most common types of cancer of the urinary tract in the world. Long non-coding RNA MALAT1 (lncR-MALAT1) is upregulated in RCC and is associated with the proliferation and migration of RCC. The present study aimed to investigate the regulating role of lncR-MALAT1 in RCC as well as the possible underlying mechanisms. The relative expression of MALAT1 and miR-22-3p in RCC tumor tissues and cell lines was detected by qRT-PCR. CCK-8 and wound healing assay were used to evaluate cell proliferation and migration ability. Western blot analysis was used to detect the expression of Ki-67, proliferating cell nuclear antigen (PCNA), matrix metalloproteinase-3 (MMP-3), migration and invasion inhibitory protein (MIIP), p-PI3K and p-Akt. The relationship between MALAT1 and miR-22-3p was examined by bioinformatic prediction analysis and luciferase reporter assay. Immunofluorescence was used to detect the activation of Akt. MALAT1 was highly expressed and the expression of miR-22-3p was suppressed in RCC tissues and cell lines. ShRNA-mediated knockdown of MALAT1 significantly inhibited the viability and mobility of RCC cells in vitro and in vivo. Further experiments revealed that miR-22-3p was a target of MALAT1 and that miR-22-3p inhibitor abolished the effect of MALAT1 shRNA on cell proliferation, migration and inactivation of PI3K/AKT pathway. In conclusion, lncR-MALAT1 affected the proliferation and migration of RCC cells by targeting miR-22-3p through the inactivation of the PI3K/Akt signaling pathway.