SF3A3, a component of the spliceosome, is involved in the RNA splicing process, a central RNA-based process commonly altered in human cancers. It plays a role in ensuring accurate splicing of mRNAs, especially those enriched for mitochondrial regulators [4]. SF3A3 is also associated with multiple biological processes such as cell cycle regulation, apoptosis, and tumorigenesis [3].

In various cancers, abnormal expression of SF3A3 has been observed. In bladder cancer, its up-regulation is correlated with poor prognosis, and overexpression promotes while depletion reduces the growth of cancer cells [1]. In non-small cell lung cancer, circSCAP binds to SF3A3, facilitating its degradation and activating the p53 signaling pathway to inhibit malignancy [2]. In acute promyelocytic leukemia, knockdown of SF3A3 suppresses the growth of NB4 cells and causes G1/S cell cycle arrest [3]. In breast cancer, its protein levels predict aggressive features, and in hepatocellular carcinoma, the STIL/FOXM1 axis activates SF3A3 to expedite cancer development [4,5].

In conclusion, SF3A3 is crucial in the spliceosome-mediated RNA splicing process. Its dysregulation significantly impacts multiple cancer-related biological processes such as cell growth, apoptosis, and cell cycle progression in various cancers including bladder, lung, leukemia, breast, and liver cancers. Research on SF3A3 provides potential therapeutic targets for these cancer types.