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      Biological function and molecular mechanism of SRSF3 in cancer and beyond

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          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.

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          Targeting autophagy in cancer

          Jean M. Mulcahy Levy, Christina Towers, Andrew Thorburn (2017)
          Autophagy is a mechanism by which cellular material is delivered to lysosomes for degradation, leading to the basal turnover of cell components and providing energy and macromolecular precursors. Autophagy has opposing, context-dependent roles in cancer, and interventions to both stimulate and inhibit autophagy have been proposed as cancer therapies. This has led to the therapeutic targeting of autophagy in cancer to be sometimes viewed as controversial. In this Review, we suggest a way forwards for the effective targeting of autophagy by understanding the context-dependent roles of autophagy and by capitalizing on modern approaches to clinical trial design.
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            Alternative Isoform Regulation in Human Tissue Transcriptomes

            Eric T Wang, Rickard Sandberg, Shujun Luo … (2008)
            Through alternative processing of pre-mRNAs, individual mammalian genes often produce multiple mRNA and protein isoforms that may have related, distinct or even opposing functions. Here we report an in-depth analysis of 15 diverse human tissue and cell line transcriptomes based on deep sequencing of cDNA fragments, yielding a digital inventory of gene and mRNA isoform expression. Analysis of mappings of sequence reads to exon-exon junctions indicated that 92-94% of human genes undergo alternative splicing (AS), ∼86% with a minor isoform frequency of 15% or more. Differences in isoform-specific read densities indicated that a majority of AS and of alternative cleavage and polyadenylation (APA) events vary between tissues, while variation between individuals was ∼2- to 3-fold less common. Extreme or ‘switch-like’ regulation of splicing between tissues was associated with increased sequence conservation in regulatory regions and with generation of full-length open reading frames. Patterns of AS and APA were strongly correlated across tissues, suggesting coordinated regulation of these processes, and sequence conservation of a subset of known regulatory motifs in both alternative introns and 3′ UTRs suggested common involvement of specific factors in tissue-level regulation of both splicing and polyadenylation.
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              Nuclear m(6)A Reader YTHDC1 Regulates mRNA Splicing.

              Wen Sara Xiao, Samir Adhikari, Ujwal Dahal … (2016)
              The regulatory role of N(6)-methyladenosine (m(6)A) and its nuclear binding protein YTHDC1 in pre-mRNA splicing remains an enigma. Here we show that YTHDC1 promotes exon inclusion in targeted mRNAs through recruiting pre-mRNA splicing factor SRSF3 (SRp20) while blocking SRSF10 (SRp38) mRNA binding. Transcriptome assay with PAR-CLIP-seq analysis revealed that YTHDC1-regulated exon-inclusion patterns were similar to those of SRSF3 but opposite of SRSF10. In vitro pull-down assay illustrated a competitive binding of SRSF3 and SRSF10 to YTHDC1. Moreover, YTHDC1 facilitates SRSF3 but represses SRSF10 in their nuclear speckle localization, RNA-binding affinity, and associated splicing events, dysregulation of which, as the result of YTHDC1 depletion, can be restored by reconstitution with wild-type, but not m(6)A-binding-defective, YTHDC1. Our findings provide the direct evidence that m(6)A reader YTHDC1 regulates mRNA splicing through recruiting and modulating pre-mRNA splicing factors for their access to the binding regions of targeted mRNAs.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Oncol Lett
                Journal ID (iso-abbrev): Oncol Lett
                Journal ID (publisher-id): OL
                Title: Oncology Letters
                Publisher: D.A. Spandidos
                ISSN (Print): 1792-1074
                ISSN (Electronic): 1792-1082
                Publication date (Print): January 2022
                Publication date (Electronic): 16 November 2021
                Publication date PMC-release: 16 November 2021
                Volume: 23
                Issue: 1
                Electronic Location Identifier: 21
                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
                Author notes
                Correspondence to: Professor Jing Sun, Institute of Medical Biotechnology, Suzhou Vocational Health College, 28 Kehua Road, Suzhou, Jiangsu 215009, P.R. China, Email: jsun@ 123456szhct.edu.cn
                Professor Weipeng Wang, Center for Drug Metabolism and Pharmacokinetics, College of Pharmaceutical Sciences, Soochow University, Yunxuan Building, 1339 Wenjing Road, Suzhou Industrial Park, Suzhou, Jiangsu 215123, P.R. China, E-mail: wangweipeng@ 123456suda.edu.cn
                [*]

                Contributed equally

                Article
                Publisher ID: OL-23-01-13139
                DOI: 10.3892/ol.2021.13139
                PMC ID: 8617561
                PubMed ID: 34858525
                SO-VID: 42a53329-bb4f-4d14-81cd-de64e19827f4
                Copyright © Copyright: © Xiong et al.
                License:

                This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

                History
                Date received : 31 March 2021
                Date accepted : 07 October 2021
                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).
                Categories
                Subject: Review

                ScienceOpen disciplines: Oncology & Radiotherapy
                Keywords: srsf3,oncogene,splicing,rna transport,post-transcriptional regulation
                Data availability:
                ScienceOpen disciplines: Oncology & Radiotherapy
                Keywords: srsf3, oncogene, splicing, rna transport, post-transcriptional regulation

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