Biological function and molecular mechanism of SRSF3 in cancer and beyond

Jian Xiong; Yinshuang Chen; Weipeng Wang; Jing Sun

doi:10.3892/ol.2021.13139

Biological function and molecular mechanism of SRSF3 in cancer and beyond

Oncol Lett. 2022 Jan;23(1):21. doi: 10.3892/ol.2021.13139. Epub 2021 Nov 16.

Authors

Jian Xiong¹, Yinshuang Chen², Weipeng Wang², Jing Sun¹

Affiliations

¹ Institute of Medical Biotechnology, Suzhou Vocational Health College, Suzhou, Jiangsu 215009, P.R. China.
² Center for Drug Metabolism and Pharmacokinetics, College of Pharmaceutical Sciences, Soochow University, Suzhou, Jiangsu 215123, P.R. China.

Abstract

Serine/arginine-rich splicing factor 3 (SRSF3; also known as SRp20), an important member of the family of SRSFs, is abnormally expressed in tumors, resulting in aberrant splicing of hub genes, such as CD44, HER2, MDM4, Rac family small GTPase 1 and tumor protein p53. Under normal conditions, the splicing and expression of SRSF3 are strictly regulated. However, the splicing, expression and phosphorylation of SRSF3 are abnormal in tumors. SRSF3 plays important roles in the occurrence and development of tumors, including the promotion of tumorigenesis, cellular proliferation, the cell cycle and metastasis, as well as inhibition of cell senescence, apoptosis and autophagy. SRSF3-knockdown significantly inhibits the proliferation and metastatic characteristics of tumor cells. Therefore, SRSF3 may be suggested as a novel anti-tumor target. The other biological functions of SRSF3 and its regulatory mechanisms are also summarized in the current review.

Keywords: RNA transport; SRSF3; oncogene; post-transcriptional regulation; splicing.

Publication types

Review

Grants and funding

Funding: The present study was supported by the National Natural Science Foundation of China (grant no. 81773044), the Science and Technology Special Project of Clinical Medicine in Jiangsu Province (grant no. BL2014046) and the Social Development Project of Jiangsu Province (grant no. BE2019657).