Background: MicroRNA(miR)-200c-3p is a tumor suppressor that helps inhibit the progression of various types of cancer. However, its role in kidney renal clear cell carcinoma (KRIC) is unknown. The purpose of this study was to explore the biological function and regulatory mechanism of miR-200c-3p in the development of KRIC.Methods: The relative levels of miR-200c-3p and vascular endothelial growth factor A (VEGFA) in KIRC tissues and cells were determined using the qRT-PCR technique. Transwell and wound healing assay methods were used to understand the effect of miR-200c-3p on the migration and invasion of 786-O and Caki-1 cells. The ability of miR-200c-3p to target VEGFA was determined using the Dual-Luciferase reporter assay system Results: MiR-200c-3p was downregulated in KIRC tissues and cell lines. The overexpression of miR-200c-3p attenuated the migratory capacities of 786-O and Caki-1 cells. The migratory ability increased under conditions of miR-200c-3p knockdown. Analysis of the results obtained using the wound healing assay revealed that overexpression of miR-200c-3p reduced the migratory abilities of Caki-1 and 786-O cells, and inhibition of miR-200c-3p accelerated the process of wound closure. Analysis of the results obtained from screening tests and by conducting the Dual-Luciferase reporter assay revealed that VEGFA was the direct target of miR-200c-3p. The VEGFA mRNA level was low in the 786-O and Caki-1 cells under conditions of overexpressed miR-200c-3p. High levels of VEGFA mRNA were observed in the cells post miR-200c-3p knockdon.Conclusions: The tumor suppression ability of miR-200c-3p in KIRC can be achieved by regulating the expression of VEGFA.