Renal cell carcinoma (RCC) serves as a prevalent malignancy of urinary system and presents severe mortality and increasing incidence. Long noncoding RNAs (lncRNAs) have demonstrated critical roles in RCC development. Here, we were interested in the function of MMP2-AS1 during RCC progression. We observed that MP2-AS1 localized in both nucleus and cytoplasm of RCC cells using fluorescent in situ hybridization (FISH). The cell viability, proliferation, invasion, and migration of RCC cells were reduced by the depletion of MMP2-AS1. The MMP2-AS1 depletion-inhibited viability, proliferation, migration, and invasion of RCC cells were rescued by the overexpression of MMP2 in vitro. Consistently, the tumor growth of RCC cells was repressed by the depletion of MMP2-AS1 in the nude mice, while the overexpression of MMP2 could reverse this effect in vivo. Mechanically, we predicted the potential interaction of miR-34c-5p with both MMP2-AS1 and MMP2. The treatment of miR-34c-5p mimic reduced the luciferase activity of MMP2-AS1 and MMP2 3'UTR. The depletion of MMP2-AS1 enhanced miR-34c-5p expression and the expression of MMP2 was inhibited by miR-34c-5p in RCC cells. The protein levels of MMP2 were downregulated by MMP2-AS1 knockdown, while the inhibitor of miR-34c-5p rescued the expression of MMP2 in the cells. The treatment of miR-34c-5p mimic attenuated the cell viability, proliferation, invasion, and migration of RCC cells, in which MMP2 overexpression restored the phenotypes. MMP2-AS1 depletion-attenuated viability, proliferation, migration, and invasion of RCC cells were reversed by miR-34c-5p inhibitor. We concluded that MMP2-AS1 contributed to progression of renal cell carcinoma by modulating miR-34c-5p/MMP2 axis.
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