Abstract
BACKGROUND: Receptor interacting protein kinase 1 (RIPK1) is crucial in the regulation of apoptosis; however, its significance in clear cell renal cell carcinoma (ccRCC) is not well understood. METHODS: Utilizing data collected from public databases, RIPK1 expression level was compared between ccRCC and control groups. The diagnostic capability of RIPK1 was confirmed by drawing receiver operating characteristic (ROC) curve. A nomogram was created based on the RIPK1 and primary clinical features of ccRCC patients. Finally, quantitative reverse transcription polymerase chain reaction (qRT-PCR) was employed to confirm the expression of RIPK1, and cell experiments including colony formation, cell counting kit8 (CCK-8), cell scratch, and Transwell assays were conducted to explore the role of RIPK1. RESULTS: The expression of RIPK1 was higher in ccRCC samples compared to normal samples (Fold-change = 0.24), which was confirmed in in vitro verification experiments. And the area under the ROC curve (AUC) values in the TCGA-ccRCC, GSE53757, and GSE66272 datasets were all greater than 0.7, indicating that RIPK1 had acceptable diagnostic ability for ccRCC patients. Then, clinical parameters such as stage, grade, and age may serve as independent prognostic indicators for ccRCC, and a nomogram was developed based on these clinical attributes and RIPK1. The AUC values of the nomogram at 1, 3, and 5 years were 0.904, 0.841, and 0.779, respectively, proving that it can effectively distinguish patients with different prognostic outcomes. According to the results of cell experiments, the RIPK1 overexpression (OE) group was associated with increased cell viability, proliferation, invasion, and migration capabilities compared to the control group. In contrast, these capabilities were markedly decreased in cells subsequent to RIPK1 knockdown (KD). CONCLUSION: The elevated expression of RIPK1 may be involved in enhancing the viability of ccRCC cells and promoting their proliferation and migration capabilities, therefore establishing a basis for clarifying the function of RIPK1 in the advancement of ccRCC. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12885-026-15728-6.