Targeting Splicing Factor SRSF6 for Cancer Therapy

Wenting She; Jun Shao; Rong Jia

doi:10.3389/fcell.2021.780023

Targeting Splicing Factor SRSF6 for Cancer Therapy

Front Cell Dev Biol. 2021 Nov 30:9:780023. doi: 10.3389/fcell.2021.780023. eCollection 2021.

Authors

Wenting She^{1

2}, Jun Shao³, Rong Jia¹

Affiliations

¹ The State Key Laboratory Breeding Base of Basic Science of Stomatology (Hubei-MOST) & Key Laboratory of Oral Biomedicine Ministry of Education, School & Hospital of Stomatology, Wuhan University, Wuhan, China.
² Department of Stomatology, Renmin Hospital of Wuhan University, Wuhan University, Wuhan, China.
³ Department of Breast Surgery, Hubei Cancer Hospital, Tongji Medical College, Huazhong University of Science and Technology and Hubei Provincial Clinical Research Center for Breast Cancer, Wuhan, China.

Abstract

Aberrant alternative splicing of pre-mRNA is an emerging cancer hallmark. Many cancer-associated genes undergo alternative splicing to produce multiple isoforms with diverse or even antagonistic functions. Oncogenic isoforms are often up-regulated, whereas tumor suppressive isoforms are down-regulated during tumorigenesis. Serine/arginine-rich splicing factor 6 (SRSF6) is an important splicing factor that regulates the alternative splicing of hundreds of target genes, including many cancer-associated genes. The potential roles of SRSF6 in cancers have attracted increasing attentions in the past decade. Accumulated pieces of evidence have shown that SRSF6 is a potential oncogenic gene that promotes oncogenic splicing when overexpressed. Targeting SRSF6 may suppress tumorigenesis. In this review, we describe the gene, mRNA, and protein structure of SRSF6; summarize the current understanding of the expression, functions, and regulatory mechanisms of SRSF6 during tumorigenesis; and discuss the potential application of targeting SRSF6 in cancer treatment.

Keywords: SRSF6; alternative splicing; cancer therapy; oncogene; overexpression.

Publication types

Review