Serine/arginine-rich splicing factors: the bridge linking alternative splicing and cancer

Xiang Zheng^2*, Qiu Peng^4*, Lujuan Wang^4*, Xuemei Zhang², Lili Huang¹, Jia Wang^3✉, Zailong Qin^1✉

1. Laboratory of Genetics and Metabolism, Maternal and Child Health Hospital of Guangxi Zhuang Autonomous Region; Guangxi Birth Defects Research and Prevention Institute, Nanning, Guangxi, 530003, China.
2. Department of Pathology, Affiliated Hospital of Guilin Medical University, Guilin, Guangxi, 541001, China.
3. Department of Immunology, Changzhi Medical College, Changzhi, Shanxi, 046000 China.
4. Cancer Research Institute, School of Basic Medical Science, Central South University, Changsha, Hunan, 410008, China.
*These authors contributed equally to this study.

This is an open access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0/). See http://ivyspring.com/terms for full terms and conditions.

Citation:
Zheng X, Peng Q, Wang L, Zhang X, Huang L, Wang J, Qin Z. Serine/arginine-rich splicing factors: the bridge linking alternative splicing and cancer. Int J Biol Sci 2020; 16(13):2442-2453. doi:10.7150/ijbs.46751. Available from https://www.ijbs.com/v16p2442.htm

Abstract

The serine/arginine-rich splicing factors (SRs) belong to the serine arginine-rich protein family, which plays an extremely important role in the splicing process of precursor RNA. The SRs recognize the splicing elements on precursor RNA, then recruit and assemble spliceosome to promote or inhibit the occurrence of splicing events. In tumors, aberrant expression of SRs causes abnormal splicing of RNA, contributing to proliferation, migration and apoptosis resistance of tumor cells. Here, we reviewed the vital role of SRs in various tumors and discussed the promise of analyzing mRNA alternative splicing events in tumor. Further, we highlight the challenges and discussed the perspectives for the identification of new potential targets for cancer therapy via SRs family members.

Keywords: serine and arginine-rich factors (SRs), SRSF, cancer, alternative splicing, splicing regulation, N6-methyladenosine (m6A), arginine methylation