Knockdown of miR-572 suppresses cell proliferation and promotes apoptosis in renal cell carcinoma cells by targeting the NF2/Hippo signaling pathway

Renal cell carcinoma (RCC) is one of the most common types of cancer. miR-572 has been proposed to be implicated in a number of human cancers, including RCC. Nevertheless, the detailed functions and molecular mechanisms of miR-572 in RCC have not been well illustrated.

The regulatory effect of miR-572 on proliferation and apoptosis is mediated through modulating NF2/Hippo signaling in RCC cell lines, providing a novel potential strategy for RCC.

qRT-PCR assay was used to assess the expression of miR-572 in RCC specimens and cell lines. Loss-of-function experiments were carried out to explore the effect of miR-572 on proliferation and apoptosis in 786-O cells. Predicted by TargetScan, the interaction between miR-572 and neurofibromin 2 (NF2) was explored by dual-luciferase reporter assay and western blot analysis. To investigate whether the regulatory effect of miR-572 was mediated by NF2, 786-O cells were transfected with anti-miR-572 alone, or together with si-NF2. After that, western blot assay was used to validate whethermiR-572 regulated proliferation and apoptosis of the RCC cell line through NF2/Hippo signaling.

miR-572 expression was upregulated in RCC specimens and cell lines, and miR-572 knockdown suppressed proliferation and enhanced apoptosis in 786-O cells. miR-572 repressed NF2 expression by binding to NF2 mRNA 3'-UTR. Moreover, the anti-miR-572-mediated regulatory effect on proliferation and apoptosis was abated by the restoration of NF2 expression in RCC cells. Furthermore, miR-572 knockdown activated NF2/Hippo signaling pathway in RCC cells. Conclusions: The regulatory effect of miR-572 on proliferation and apoptosis is mediated through modulating NF2/Hippo signaling in RCC cell lines, providing a novel potential strategy for RCC.