BACKGROUND: Renal cell carcinoma (RCC) exhibits malignant biological characteristics of cell invasion and metastasis. The role of regulator of cullins-1 (ROC1) in RCC is unknown. The present work focused on exploring ROC1's biological effect on RCC as well as clarifying its related mechanism. METHODS: The messenger RNA (mRNA) expression of ROC1 in RCC tumor tissue and normal tissue was examined by reverse transcription-polymerase chain reaction (RT-PCR). We analyzed mRNA expression through RT-PCR, whereas protein level via western blot (WB) assay. We did some biological experiments in this study, including Cell Counting Kit-8 (CCK-8) assay, 5-ethynyl-2'-deoxyuridine (EdU) assay, Transwell invasion assay, and xenograft tumor assay. RESULTS: ROC1 expression markedly increased in the RCC samples relative to healthy samples. ROC1 was related to the dismal outcome of RCC patients. We also found that the overexpression of ROC1 (oeROC1) promoted cell proliferation, epithelial-mesenchymal transition (EMT), and invasion, whereas ROC1 interference had opposite effects. ROC1 regulated GSK-3β/Wnt pathway within RCC cells. By constructing the RCC metastasis model in nude mice, it was found that ROC1 knockdown inhibited tumor metastasis, while shGSK-3β could reverse the effect of ROC1 knockdown. CONCLUSIONS: Collectively, our work preliminarily illuminated the tumor-promoting role of ROC1 in RCC and the potential molecular mechanism. Thus, our study may provide some evidence for the treatment of RCC.