Objective The aim of this study is to assess the antitumor properties and associated molecular mechanisms of lidocaine on renal cell carcinoma (RCC) A498 cells under in vitro conditions. Methods RCC A498 cells were exposed to varying concentrations of lidocaine (0, 0.1, 0.5, 1, 2, and 5 mM) for 24, 48, and 72 h. Cell viability was assessed using the Cell Counting Kit-8 assay to identify effective concentrations. Based on these results, further experiments were conducted using lidocaine at 0, 0.1, 0.5, and 1 mM for 48 h. Apoptotic changes were evaluated using a double-staining apoptosis detection kit, followed by analysis through flow cytometry. Cell migration was assessed using a 24-h Transwell migration assay. Quantitative real-time polymerase chain reaction (qRT-PCR) was employed to measure mRNA expression levels CASP3, CASP8, CASP9, and ACTB. Protein expression levels of BCL2-associated X protein (Bax), B-cell lymphoma-2 (Bcl-2), Caspase-3, Caspase-8, and Caspase-9 were examined through immunoblotting following treatment with 1 mM lidocaine for 48 h. Results Lidocaine inhibited A498 cell viability in a dose- and time-dependent manner. A reduction in migratory activity was observed with increasing lidocaine concentrations. Flow cytometric analysis demonstrated significantly elevated apoptosis rates at 0.1, 0.5, and 1 mM lidocaine compared to untreated controls (p < 0.05). qRT-PCR analysis demonstrated upregulation of CASP3, CASP8, and CASP9 transcripts. Western blot results confirmed increased protein expression of Bax, Caspase-3, and Caspase-9, along with decreased Bcl-2 levels. Conclusion Lidocaine exhibited antitumor activity against RCC A498 cells in vitro by suppressing proliferation, inhibiting migration, and promoting apoptosis via activation of caspase-dependent pathways.