Purpose <p>Tumor-derived extracellular vesicles (EVs) can deliver microRNAs (miRNAs) to promote tumor development. Herein, this study explored whether tumor-derived EVs carrying miR-671-5p facilitated renal cell carcinoma (RCC) cell growth.</p> Methods <p>miR-671-5p expression in RCC cells and the collected EVs was assessed. After gain- and loss-of-function assays and EV co-culture, cell viability, invasion and migration, and apoptosis were measured. RNA pull-down and dual-luciferase reporter assays were used to analyze the binding between miR-671-5p and inhibitor of growth 5 (ING5). The function of EVs in RCC metastasis in vivo was evaluated through tumor transplantation in nude mice.</p> Results <p>miR-671-5p was up-regulated in RCC cells and EVs from ACHN cells. miR-671-5p down-regulation inhibited RCC cell proliferation, invasion, and migration but accelerated cell apoptosis. EVs derived from ACHN cells carried miR-671-5p into RCC cells. RCC cell invasion, migration, and proliferation were diminished but cell apoptosis was elevated after co-culture with EVs carrying inhibitors-miR-671-5p. Mechanistically, ING5 was a target of miR-671-5p. ING5 silencing abrogated the effects of EVs carrying inhibitors-miR-671-5p on RCC cells. EVs accelerated tumor growth, increased tumor volume, and elevated Ki-67-positive cells in mice, accompanied by increased miR-671-5p expression and decreased ING5 expression, whereas EVs carrying inhibitors-miR-671-5p contributed to opposite results.</p> Conclusion <p>Tumor-derived EVs carrying miR-671-5p target ING5 to promote RCC cell growth.</p> Graphical abstract <p></p>