Preliminary exploration of the putative function of SF3A2 in clear cell renal cell carcinoma

Splicing factor 3a subunit 2 (SF3A2) has been implicated in an increasing number of tumor types; however, at present, its role in clear cell renal cell carcinoma (ccRCC) has yet to be fully elucidated. Therefore, the aim of the present study was to preliminarily explore the putative function of SF3A2 in ccRCC. To meet this aim, SF3A2 expression in ccRCC tissues was analyzed using The Cancer Genome Atlas Kidney Renal Clear Cell Carcinoma dataset and conducted reverse transcription‑quantitative PCR, western blotting and immunohistochemical staining of ccRCC cell models to validate its functional roles. To evaluate the impact of SF3A2 expression on the proliferation, migration and invasion of ccRCC cells, Cell Counting Kit‑8 assays, colony formation assays, Transwell assays and an <i>in vivo</i> xenograft model were employed. Furthermore, western blot analysis was performed to explore which proteins may be involved in the underlying mechanisms of the effects of SF3A2 in ccRCC progression. SF3A2 was found to be markedly upregulated in ccRCC cells and tissues, and its high expression was associated with poor prognosis. The functional assays and <i>in vivo</i> experiments revealed that SF3A2 knockdown inhibited the proliferation, migration and invasion of the ccRCC cells, whereas its overexpression enhanced these processes. In terms of the underlying mechanism, SF3A2 was shown to promote ccRCC progression via activation of the AKT signaling pathway. In conclusion, the present study identified SF3A2 upregulation as a prognostic marker in ccRCC, which was associated with poor clinical outcomes and accelerated tumor progression. Mechanistically, SF3A2 exerted tumor‑promoting effects through the AKT signaling pathway. Taken together, these findings positioned SF3A2 as a dual‑functional biomarker with translational potential, facilitating prognostic stratification and presenting therapeutic targeting opportunities for ccRCC management.