SF3A3, a component of the spliceosome, plays a crucial role in RNA splicing, an essential process for gene expression regulation. It is involved in various biological pathways and its proper function is of great biological importance. Genetic models, such as KO or CKO mouse models, can be valuable in studying its function [1-10].

In cancer research, abnormal SF3A3 expression is related to the development of multiple cancers. In bladder cancer, its up-regulation is correlated with poor prognosis, and depletion of SF3A3 reduces cancer cell growth in vivo and vitro [1]. In non-small cell lung cancer, circSCAP binds to SF3A3, promoting its degradation and activating p53 signaling to inhibit malignancy [2]. In acute promyelocytic leukemia, knockdown of SF3A3 suppresses cell growth, causing G1/S cell cycle arrest [3]. In breast cancer, SF3A3 levels are translationally modulated by MYC, leading to metabolic reprogramming and stem-like properties [4]. In hepatocellular carcinoma, down-regulation of SF3A3 inhibits the malignant behavior of HCC cells [5].

In conclusion, SF3A3 is essential for RNA splicing and is involved in various biological processes. Its dysregulation contributes to the development of multiple cancers, as revealed by functional studies including those using potential gene-knockout-like models. Understanding SF3A3 function provides insights into cancer mechanisms and potential therapeutic targets.

References:

1. Liu, Kai-Long, Yin, Yue-Wei, Lu, Bao-Sai, Yang, Zhan, Li, Wei. 2022. E2F6/KDM5C promotes SF3A3 expression and bladder cancer progression through a specific hypomethylated DNA promoter. In Cancer cell international, 22, 109. doi:10.1186/s12935-022-02475-4. https://pubmed.ncbi.nlm.nih.gov/35248043/

2. Chen, Dongni, Zhou, Hongli, Cai, Zhuochen, Wang, Hui-Yun, Wen, Zhesheng. 2022. CircSCAP interacts with SF3A3 to inhibit the malignance of non-small cell lung cancer by activating p53 signaling. In Journal of experimental & clinical cancer research : CR, 41, 120. doi:10.1186/s13046-022-02299-0. https://pubmed.ncbi.nlm.nih.gov/35365208/

3. Chang, Jiayin, Yan, Shihai, Geng, Zhirong, Wang, Zhilin. 2023. Inhibition of splicing factors SF3A3 and SRSF5 contributes to As3+/Se4+ combination-mediated proliferation suppression and apoptosis induction in acute promyelocytic leukemia cells. In Archives of biochemistry and biophysics, 743, 109677. doi:10.1016/j.abb.2023.109677. https://pubmed.ncbi.nlm.nih.gov/37356608/

4. Cieśla, Maciej, Ngoc, Phuong Cao Thi, Cordero, Eugenia, Bosch, Ana, Bellodi, Cristian. 2021. Oncogenic translation directs spliceosome dynamics revealing an integral role for SF3A3 in breast cancer. In Molecular cell, 81, 1453-1468.e12. doi:10.1016/j.molcel.2021.01.034. https://pubmed.ncbi.nlm.nih.gov/33662273/

5. Zhang, Haijun, Zhang, Lin, Wu, Ziqi. 2025. Interaction of STIL with FOXM1 regulates SF3A3 transcription in the hepatocellular carcinoma development. In Cell division, 20, 1. doi:10.1186/s13008-025-00142-4. https://pubmed.ncbi.nlm.nih.gov/39825314/