This study investigated the potential mechanism through which lathyrol (Lat) regulates heterogeneous nuclear ribonucleoprotein K (hnRNP K) to influence the proliferation and apoptosis of renal carcinoma Renca cells. Logarithmically growing Renca cells were divided into a model group (Mod), a Lat group, and a cisplatin(DDP) group. The proliferation of cells at various drug concentrations was evaluated using CCK-8 assay, and the optimal concentration was selected for subsequent experiments. Cell-based and mouse xenograft tumor models were established, with group settings consistent with the in vitro experiments. Western blot analysis was employed to detect the expression levels of hnRNP K, Ki-67, B-cell lymphoma-2 (BCL-2), and BCL-2 associated X protein (BAX) in renal carcinoma Renca cells and tumor tissues from the mouse models. HE staining assessed morphological changes in xenograft tumor tissues. Immunohistochemistry was conducted to evaluate the expression of proliferating cell nuclear antigen (PCNA), cysteinyl aspartate specific proteinase-3 (Caspase-3), and Caspase-9. TUNEL assay was performed to quantify the apoptotic rate in xenograft tumor tissues. The results demonstrated that Lat and DDP significantly downregulated the expression of hnRNP K, Ki-67, PCNA, and BCL-2 in renal carcinoma Renca cells and mouse xenograft tumor tissues, with corresponding upregulation of BAX, Caspase-3, and Caspase-9 (all P < 0.05). In the Lat group, tumor cell proliferation was suppressed, nuclear condensation and fragmentation were observed, and the proportion of TUNEL-positive cells significantly increased (P < 0.001). These findings suggest that Lat may suppress proliferation and promote apoptosis in renal cancer Renca cells by down-regulating hnRNP K expression.