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The Clinical Role of SRSF1 Expression in Cancer: A Review of the Current Literature
Background: SFRS1 is a member of the splicing factor protein family. Through a specific sequence of alteration, SRSF1 can move from the cytoplasm to the nucleus where it can work autonomously as a splicing activator, or as a silencer when interacting with other regulators. Alternative splicing (AS)...
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Published in: | Applied sciences 2022-03, Vol.12 (5), p.2268 |
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creator | Lo Giudice, Arturo Asmundo, Maria Giovanna Broggi, Giuseppe Cimino, Sebastiano Morgia, Giuseppe Di Trapani, Ettore Luzzago, Stefano Musi, Gennaro Ferro, Matteo de Cobelli, Ottavio Russo, Giorgio I. |
description | Background: SFRS1 is a member of the splicing factor protein family. Through a specific sequence of alteration, SRSF1 can move from the cytoplasm to the nucleus where it can work autonomously as a splicing activator, or as a silencer when interacting with other regulators. Alternative splicing (AS) is a fundamental biological process that ensures protein diversity. In fact, different proteins, produced by alternative splicing, can gain different and even antagonistic biological functions. Methods: Our review is based on English articles published in the MEDLINE/PubMed medical library between 2000 and 2021. We retrieved articles that were specifically related to SRSF1 and cancers, and we excluded other reviews and meta-analyses. We included in vitro studies, animal studies and clinical studies, evaluated using the Medical Education Research Study Quality Instrument (MERSQI) and the Newcastle–Ottawa Scale-Education (NOSE). Result: SRSF1 is related to various genes and plays a role in cell cycle, ubiquitin-mediated proteolysis, nucleotide excision repair, p53 pathway, apoptosis, DNA replication and RNA degradation. In most cases, SRSF1 carries out its cancer-related function via abnormal alternative splicing (AS). However, according to the most recent literature, SRSF1 may also be involved in mRNA translation and cancer chemoresistance or radio-sensitivity. Conclusion: Our results showed that SRSF1 plays a key clinical role in tumorigenesis and tumor progression in several types of cancer (such as Prostate, Lung, Breast, Colon, Glioblastoma), through various mechanisms of action and different cellular pathways. This review could be a starting point for several studies regarding the biology of and therapies for cancer. |
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Through a specific sequence of alteration, SRSF1 can move from the cytoplasm to the nucleus where it can work autonomously as a splicing activator, or as a silencer when interacting with other regulators. Alternative splicing (AS) is a fundamental biological process that ensures protein diversity. In fact, different proteins, produced by alternative splicing, can gain different and even antagonistic biological functions. Methods: Our review is based on English articles published in the MEDLINE/PubMed medical library between 2000 and 2021. We retrieved articles that were specifically related to SRSF1 and cancers, and we excluded other reviews and meta-analyses. We included in vitro studies, animal studies and clinical studies, evaluated using the Medical Education Research Study Quality Instrument (MERSQI) and the Newcastle–Ottawa Scale-Education (NOSE). Result: SRSF1 is related to various genes and plays a role in cell cycle, ubiquitin-mediated proteolysis, nucleotide excision repair, p53 pathway, apoptosis, DNA replication and RNA degradation. In most cases, SRSF1 carries out its cancer-related function via abnormal alternative splicing (AS). However, according to the most recent literature, SRSF1 may also be involved in mRNA translation and cancer chemoresistance or radio-sensitivity. Conclusion: Our results showed that SRSF1 plays a key clinical role in tumorigenesis and tumor progression in several types of cancer (such as Prostate, Lung, Breast, Colon, Glioblastoma), through various mechanisms of action and different cellular pathways. This review could be a starting point for several studies regarding the biology of and therapies for cancer.</description><identifier>ISSN: 2076-3417</identifier><identifier>EISSN: 2076-3417</identifier><identifier>DOI: 10.3390/app12052268</identifier><language>eng</language><publisher>Basel: MDPI AG</publisher><subject>Alternative splicing ; Apoptosis ; Biological activity ; Breast ; Breast cancer ; Cell cycle ; Chemoresistance ; Colon ; Cyclin-dependent kinases ; Cytoplasm ; DNA biosynthesis ; DNA repair ; Education ; Gene expression ; Genomes ; Glioblastoma ; Kinases ; Literature reviews ; lung ; Lung cancer ; Medical libraries ; Medical prognosis ; Medical research ; mRNA ; Nucleotide excision repair ; Nucleotides ; p53 Protein ; Phosphorylation ; prostate ; Prostate cancer ; Proteins ; Proteolysis ; Regulatory sequences ; Splicing ; Splicing factors ; SRSF1 ; Survival analysis ; Tumorigenesis ; Ubiquitin</subject><ispartof>Applied sciences, 2022-03, Vol.12 (5), p.2268</ispartof><rights>2022 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c364t-5c8a201f1ab127e95d361a2899c0e4b1c9b7bcc21a928c0e9a700697bff7e0363</citedby><cites>FETCH-LOGICAL-c364t-5c8a201f1ab127e95d361a2899c0e4b1c9b7bcc21a928c0e9a700697bff7e0363</cites><orcidid>0000-0003-4687-7353 ; 0000-0003-2576-6523 ; 0000-0003-1987-929X ; 0000-0002-9250-7858</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.proquest.com/docview/2637582602/fulltextPDF?pq-origsite=primo$$EPDF$$P50$$Gproquest$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/2637582602?pq-origsite=primo$$EHTML$$P50$$Gproquest$$Hfree_for_read</linktohtml><link.rule.ids>314,780,784,25753,27924,27925,37012,44590,75126</link.rule.ids></links><search><creatorcontrib>Lo Giudice, Arturo</creatorcontrib><creatorcontrib>Asmundo, Maria Giovanna</creatorcontrib><creatorcontrib>Broggi, Giuseppe</creatorcontrib><creatorcontrib>Cimino, Sebastiano</creatorcontrib><creatorcontrib>Morgia, Giuseppe</creatorcontrib><creatorcontrib>Di Trapani, Ettore</creatorcontrib><creatorcontrib>Luzzago, Stefano</creatorcontrib><creatorcontrib>Musi, Gennaro</creatorcontrib><creatorcontrib>Ferro, Matteo</creatorcontrib><creatorcontrib>de Cobelli, Ottavio</creatorcontrib><creatorcontrib>Russo, Giorgio I.</creatorcontrib><title>The Clinical Role of SRSF1 Expression in Cancer: A Review of the Current Literature</title><title>Applied sciences</title><description>Background: SFRS1 is a member of the splicing factor protein family. Through a specific sequence of alteration, SRSF1 can move from the cytoplasm to the nucleus where it can work autonomously as a splicing activator, or as a silencer when interacting with other regulators. Alternative splicing (AS) is a fundamental biological process that ensures protein diversity. In fact, different proteins, produced by alternative splicing, can gain different and even antagonistic biological functions. Methods: Our review is based on English articles published in the MEDLINE/PubMed medical library between 2000 and 2021. We retrieved articles that were specifically related to SRSF1 and cancers, and we excluded other reviews and meta-analyses. We included in vitro studies, animal studies and clinical studies, evaluated using the Medical Education Research Study Quality Instrument (MERSQI) and the Newcastle–Ottawa Scale-Education (NOSE). Result: SRSF1 is related to various genes and plays a role in cell cycle, ubiquitin-mediated proteolysis, nucleotide excision repair, p53 pathway, apoptosis, DNA replication and RNA degradation. In most cases, SRSF1 carries out its cancer-related function via abnormal alternative splicing (AS). However, according to the most recent literature, SRSF1 may also be involved in mRNA translation and cancer chemoresistance or radio-sensitivity. Conclusion: Our results showed that SRSF1 plays a key clinical role in tumorigenesis and tumor progression in several types of cancer (such as Prostate, Lung, Breast, Colon, Glioblastoma), through various mechanisms of action and different cellular pathways. This review could be a starting point for several studies regarding the biology of and therapies for cancer.</description><subject>Alternative splicing</subject><subject>Apoptosis</subject><subject>Biological activity</subject><subject>Breast</subject><subject>Breast cancer</subject><subject>Cell cycle</subject><subject>Chemoresistance</subject><subject>Colon</subject><subject>Cyclin-dependent kinases</subject><subject>Cytoplasm</subject><subject>DNA biosynthesis</subject><subject>DNA repair</subject><subject>Education</subject><subject>Gene expression</subject><subject>Genomes</subject><subject>Glioblastoma</subject><subject>Kinases</subject><subject>Literature reviews</subject><subject>lung</subject><subject>Lung cancer</subject><subject>Medical libraries</subject><subject>Medical prognosis</subject><subject>Medical research</subject><subject>mRNA</subject><subject>Nucleotide excision repair</subject><subject>Nucleotides</subject><subject>p53 Protein</subject><subject>Phosphorylation</subject><subject>prostate</subject><subject>Prostate cancer</subject><subject>Proteins</subject><subject>Proteolysis</subject><subject>Regulatory sequences</subject><subject>Splicing</subject><subject>Splicing factors</subject><subject>SRSF1</subject><subject>Survival analysis</subject><subject>Tumorigenesis</subject><subject>Ubiquitin</subject><issn>2076-3417</issn><issn>2076-3417</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><sourceid>PIMPY</sourceid><sourceid>DOA</sourceid><recordid>eNpNUV1Lw0AQDKJgqX3yDxz4KNH7SO7Dt1JaLRSEtj4fm-tGr8RcvCR-_HtTK-K-7DLMzgxMklwyeiOEobfQNIzTnHOpT5IRp0qmImPq9N99nkzadk-HMUxoRkfJZvuCZFb52juoyDpUSEJJNuvNgpH5ZxOxbX2oia_JDGqH8Y5MyRrfPX4ceN3huY8R646sfIcRuj7iRXJWQtXi5HePk6fFfDt7SFeP98vZdJU6IbMuzZ0GTlnJoGBcocl3QjLg2hhHMSuYM4UqnOMMDNcDZEBRKo0qylIhFVKMk-VRdxdgb5voXyF-2QDe_gAhPluInXcVWiWV4xoN7kqd5RlqmeFgm2kqNADCoHV11GpieOux7ew-9LEe4lsuhco1l5QPrOsjy8XQthHLP1dG7aEE-68E8Q19D3c5</recordid><startdate>20220301</startdate><enddate>20220301</enddate><creator>Lo Giudice, Arturo</creator><creator>Asmundo, Maria Giovanna</creator><creator>Broggi, Giuseppe</creator><creator>Cimino, Sebastiano</creator><creator>Morgia, Giuseppe</creator><creator>Di Trapani, Ettore</creator><creator>Luzzago, Stefano</creator><creator>Musi, Gennaro</creator><creator>Ferro, Matteo</creator><creator>de Cobelli, Ottavio</creator><creator>Russo, Giorgio I.</creator><general>MDPI AG</general><scope>AAYXX</scope><scope>CITATION</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>DOA</scope><orcidid>https://orcid.org/0000-0003-4687-7353</orcidid><orcidid>https://orcid.org/0000-0003-2576-6523</orcidid><orcidid>https://orcid.org/0000-0003-1987-929X</orcidid><orcidid>https://orcid.org/0000-0002-9250-7858</orcidid></search><sort><creationdate>20220301</creationdate><title>The Clinical Role of SRSF1 Expression in Cancer: A Review of the Current Literature</title><author>Lo Giudice, Arturo ; Asmundo, Maria Giovanna ; Broggi, Giuseppe ; Cimino, Sebastiano ; Morgia, Giuseppe ; Di Trapani, Ettore ; Luzzago, Stefano ; Musi, Gennaro ; Ferro, Matteo ; de Cobelli, Ottavio ; Russo, Giorgio I.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c364t-5c8a201f1ab127e95d361a2899c0e4b1c9b7bcc21a928c0e9a700697bff7e0363</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>Alternative splicing</topic><topic>Apoptosis</topic><topic>Biological activity</topic><topic>Breast</topic><topic>Breast cancer</topic><topic>Cell cycle</topic><topic>Chemoresistance</topic><topic>Colon</topic><topic>Cyclin-dependent kinases</topic><topic>Cytoplasm</topic><topic>DNA biosynthesis</topic><topic>DNA repair</topic><topic>Education</topic><topic>Gene expression</topic><topic>Genomes</topic><topic>Glioblastoma</topic><topic>Kinases</topic><topic>Literature reviews</topic><topic>lung</topic><topic>Lung cancer</topic><topic>Medical libraries</topic><topic>Medical prognosis</topic><topic>Medical research</topic><topic>mRNA</topic><topic>Nucleotide excision repair</topic><topic>Nucleotides</topic><topic>p53 Protein</topic><topic>Phosphorylation</topic><topic>prostate</topic><topic>Prostate cancer</topic><topic>Proteins</topic><topic>Proteolysis</topic><topic>Regulatory sequences</topic><topic>Splicing</topic><topic>Splicing factors</topic><topic>SRSF1</topic><topic>Survival analysis</topic><topic>Tumorigenesis</topic><topic>Ubiquitin</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lo Giudice, Arturo</creatorcontrib><creatorcontrib>Asmundo, Maria Giovanna</creatorcontrib><creatorcontrib>Broggi, Giuseppe</creatorcontrib><creatorcontrib>Cimino, Sebastiano</creatorcontrib><creatorcontrib>Morgia, Giuseppe</creatorcontrib><creatorcontrib>Di Trapani, Ettore</creatorcontrib><creatorcontrib>Luzzago, Stefano</creatorcontrib><creatorcontrib>Musi, Gennaro</creatorcontrib><creatorcontrib>Ferro, Matteo</creatorcontrib><creatorcontrib>de Cobelli, Ottavio</creatorcontrib><creatorcontrib>Russo, Giorgio I.</creatorcontrib><collection>CrossRef</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central</collection><collection>ProQuest Central Essentials</collection><collection>AUTh Library subscriptions: ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central</collection><collection>Publicly Available Content Database (Proquest) (PQ_SDU_P3)</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>Applied sciences</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lo Giudice, Arturo</au><au>Asmundo, Maria Giovanna</au><au>Broggi, Giuseppe</au><au>Cimino, Sebastiano</au><au>Morgia, Giuseppe</au><au>Di Trapani, Ettore</au><au>Luzzago, Stefano</au><au>Musi, Gennaro</au><au>Ferro, Matteo</au><au>de Cobelli, Ottavio</au><au>Russo, Giorgio I.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The Clinical Role of SRSF1 Expression in Cancer: A Review of the Current Literature</atitle><jtitle>Applied sciences</jtitle><date>2022-03-01</date><risdate>2022</risdate><volume>12</volume><issue>5</issue><spage>2268</spage><pages>2268-</pages><issn>2076-3417</issn><eissn>2076-3417</eissn><abstract>Background: SFRS1 is a member of the splicing factor protein family. Through a specific sequence of alteration, SRSF1 can move from the cytoplasm to the nucleus where it can work autonomously as a splicing activator, or as a silencer when interacting with other regulators. Alternative splicing (AS) is a fundamental biological process that ensures protein diversity. In fact, different proteins, produced by alternative splicing, can gain different and even antagonistic biological functions. Methods: Our review is based on English articles published in the MEDLINE/PubMed medical library between 2000 and 2021. We retrieved articles that were specifically related to SRSF1 and cancers, and we excluded other reviews and meta-analyses. We included in vitro studies, animal studies and clinical studies, evaluated using the Medical Education Research Study Quality Instrument (MERSQI) and the Newcastle–Ottawa Scale-Education (NOSE). Result: SRSF1 is related to various genes and plays a role in cell cycle, ubiquitin-mediated proteolysis, nucleotide excision repair, p53 pathway, apoptosis, DNA replication and RNA degradation. In most cases, SRSF1 carries out its cancer-related function via abnormal alternative splicing (AS). However, according to the most recent literature, SRSF1 may also be involved in mRNA translation and cancer chemoresistance or radio-sensitivity. Conclusion: Our results showed that SRSF1 plays a key clinical role in tumorigenesis and tumor progression in several types of cancer (such as Prostate, Lung, Breast, Colon, Glioblastoma), through various mechanisms of action and different cellular pathways. 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subjects | Alternative splicing Apoptosis Biological activity Breast Breast cancer Cell cycle Chemoresistance Colon Cyclin-dependent kinases Cytoplasm DNA biosynthesis DNA repair Education Gene expression Genomes Glioblastoma Kinases Literature reviews lung Lung cancer Medical libraries Medical prognosis Medical research mRNA Nucleotide excision repair Nucleotides p53 Protein Phosphorylation prostate Prostate cancer Proteins Proteolysis Regulatory sequences Splicing Splicing factors SRSF1 Survival analysis Tumorigenesis Ubiquitin |
title | The Clinical Role of SRSF1 Expression in Cancer: A Review of the Current Literature |
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