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Somatic nuclear auto-antigenic sperm protein sensitizes human breast cancer cells to 5-Fluorouracil
Purpose To assess the potential role of nuclear auto-antigenic sperm protein (NASP) in the cellular sensitivity to 5-Fluorouracil (5-FU) in breast cancer cells. Methods The expression of two NASP isotypes, namely somatic NASP (sNASP) and testis NASP (tNASP) in breast cancer lines were detected under...
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| Published in: | Cancer chemotherapy and pharmacology 2022-04, Vol.89 (4), p.559-564 |
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| container_end_page | 564 |
| container_issue | 4 |
| container_start_page | 559 |
| container_title | Cancer chemotherapy and pharmacology |
| container_volume | 89 |
| creator | Huang, Yanjing Yang, Shenghui Yu, Weiling Gui, Ling |
| description | Purpose
To assess the potential role of nuclear auto-antigenic sperm protein (NASP) in the cellular sensitivity to 5-Fluorouracil (5-FU) in breast cancer cells.
Methods
The expression of two NASP isotypes, namely somatic NASP (sNASP) and testis NASP (tNASP) in breast cancer lines were detected under 5-FU treatment using real-time polymerase chain reaction and western blot assays. NASP effect on cellular viability and apoptosis under 5-FU treatment were evaluated. The interaction between NASP and its downstream proteins were evaluated using the co-immunoprecipitation (Co-IP) assays.
Results
5-FU significantly decreased the mRNA and protein expression levels of sNASP. Inhibition of sNASP increased cellular viability, colony formation ability, but reduced apoptosis in tested cell lines in response to 5-FU, which were reversed by sNASP over-expression. Further study reveals 5-FU disrupts sNASP/TNF receptor-associated factor 6 (TRAF6) complex, potentiates cellular sensitivity to 5-FU via NK-kB.
Conclusion
Our findings suggest sNASP is a novel molecular target having potential to overcome the resistance to 5-FU in breast cancer cells. |
| doi_str_mv | 10.1007/s00280-021-04391-2 |
| format | article |
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To assess the potential role of nuclear auto-antigenic sperm protein (NASP) in the cellular sensitivity to 5-Fluorouracil (5-FU) in breast cancer cells.
Methods
The expression of two NASP isotypes, namely somatic NASP (sNASP) and testis NASP (tNASP) in breast cancer lines were detected under 5-FU treatment using real-time polymerase chain reaction and western blot assays. NASP effect on cellular viability and apoptosis under 5-FU treatment were evaluated. The interaction between NASP and its downstream proteins were evaluated using the co-immunoprecipitation (Co-IP) assays.
Results
5-FU significantly decreased the mRNA and protein expression levels of sNASP. Inhibition of sNASP increased cellular viability, colony formation ability, but reduced apoptosis in tested cell lines in response to 5-FU, which were reversed by sNASP over-expression. Further study reveals 5-FU disrupts sNASP/TNF receptor-associated factor 6 (TRAF6) complex, potentiates cellular sensitivity to 5-FU via NK-kB.
Conclusion
Our findings suggest sNASP is a novel molecular target having potential to overcome the resistance to 5-FU in breast cancer cells.</description><identifier>ISSN: 0344-5704</identifier><identifier>EISSN: 1432-0843</identifier><identifier>DOI: 10.1007/s00280-021-04391-2</identifier><identifier>PMID: 35133490</identifier><language>eng</language><publisher>Berlin/Heidelberg: Springer Berlin Heidelberg</publisher><subject>5-Fluorouracil ; Antigens ; Antigens, Nuclear ; Apoptosis ; Breast cancer ; Breast Neoplasms - drug therapy ; Cancer Research ; Cell Line, Tumor ; Cell Survival ; Cell viability ; Drug Resistance, Neoplasm ; Evaluation ; Fluorouracil - pharmacology ; Gene expression ; Humans ; Immunoprecipitation ; Isotypes ; Male ; Medicine ; Medicine & Public Health ; mRNA ; Oncology ; Overexpression ; Pharmacology/Toxicology ; Polymerase chain reaction ; Proteins ; Sensitivity ; Short Communication ; Sperm ; Spermatozoa ; TRAF6 protein ; Tumor necrosis factor ; Tumor necrosis factor receptors</subject><ispartof>Cancer chemotherapy and pharmacology, 2022-04, Vol.89 (4), p.559-564</ispartof><rights>The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature 2022</rights><rights>2022. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.</rights><rights>The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature 2022.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c326t-e2521b15da696be0bb2fcf564a08f2136997f4f185e604be4b124b29bda9c86a3</cites><orcidid>0000-0001-5255-7589</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/35133490$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Huang, Yanjing</creatorcontrib><creatorcontrib>Yang, Shenghui</creatorcontrib><creatorcontrib>Yu, Weiling</creatorcontrib><creatorcontrib>Gui, Ling</creatorcontrib><title>Somatic nuclear auto-antigenic sperm protein sensitizes human breast cancer cells to 5-Fluorouracil</title><title>Cancer chemotherapy and pharmacology</title><addtitle>Cancer Chemother Pharmacol</addtitle><addtitle>Cancer Chemother Pharmacol</addtitle><description>Purpose
To assess the potential role of nuclear auto-antigenic sperm protein (NASP) in the cellular sensitivity to 5-Fluorouracil (5-FU) in breast cancer cells.
Methods
The expression of two NASP isotypes, namely somatic NASP (sNASP) and testis NASP (tNASP) in breast cancer lines were detected under 5-FU treatment using real-time polymerase chain reaction and western blot assays. NASP effect on cellular viability and apoptosis under 5-FU treatment were evaluated. The interaction between NASP and its downstream proteins were evaluated using the co-immunoprecipitation (Co-IP) assays.
Results
5-FU significantly decreased the mRNA and protein expression levels of sNASP. Inhibition of sNASP increased cellular viability, colony formation ability, but reduced apoptosis in tested cell lines in response to 5-FU, which were reversed by sNASP over-expression. Further study reveals 5-FU disrupts sNASP/TNF receptor-associated factor 6 (TRAF6) complex, potentiates cellular sensitivity to 5-FU via NK-kB.
Conclusion
Our findings suggest sNASP is a novel molecular target having potential to overcome the resistance to 5-FU in breast cancer cells.</description><subject>5-Fluorouracil</subject><subject>Antigens</subject><subject>Antigens, Nuclear</subject><subject>Apoptosis</subject><subject>Breast cancer</subject><subject>Breast Neoplasms - drug therapy</subject><subject>Cancer Research</subject><subject>Cell Line, Tumor</subject><subject>Cell Survival</subject><subject>Cell viability</subject><subject>Drug Resistance, Neoplasm</subject><subject>Evaluation</subject><subject>Fluorouracil - pharmacology</subject><subject>Gene expression</subject><subject>Humans</subject><subject>Immunoprecipitation</subject><subject>Isotypes</subject><subject>Male</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>mRNA</subject><subject>Oncology</subject><subject>Overexpression</subject><subject>Pharmacology/Toxicology</subject><subject>Polymerase chain reaction</subject><subject>Proteins</subject><subject>Sensitivity</subject><subject>Short Communication</subject><subject>Sperm</subject><subject>Spermatozoa</subject><subject>TRAF6 protein</subject><subject>Tumor necrosis factor</subject><subject>Tumor necrosis factor receptors</subject><issn>0344-5704</issn><issn>1432-0843</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><recordid>eNp9kU9PHDEMxaOqVVm2_QI9VJF66SXUcTLZmSNCUJCQOBTOUZL10EEzmSXJHMqnb-jyR-qBkyX75-cnP8a-SDiSAJsfGQBbEIBSgFadFPiOraRWKKDV6j1bgdJaNBvQB-ww5zsA0FKpj-xANbXqDlYs_JonV4bA4xJGcom7pczCxTLcUqztvKM08V2aCw2RZ4p5KMMDZf57mVzkPpHLhQcXAyUeaBwzLzNvxNm4zGlekgvD-Il96N2Y6fNTXbObs9Prk3NxefXz4uT4UgSFpgjCBqWXzdaZzngC77EPfWO0g7ZHqUzXbXrdy7YhA9qT9hK1x85vXRda49Safd_rVrv3C-VipyE_enKR5iVbNGjaDlR91pp9-w-9q2ZjdVcprSTixqhK4Z4Kac45UW93aZhc-mMl2McI7D4CWyOw_yKwWJe-PkkvfqLty8rzzyug9kCuo3hL6fX2G7J_AS5BkZ4</recordid><startdate>20220401</startdate><enddate>20220401</enddate><creator>Huang, Yanjing</creator><creator>Yang, Shenghui</creator><creator>Yu, Weiling</creator><creator>Gui, Ling</creator><general>Springer Berlin Heidelberg</general><general>Springer Nature B.V</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7TO</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>H94</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0001-5255-7589</orcidid></search><sort><creationdate>20220401</creationdate><title>Somatic nuclear auto-antigenic sperm protein sensitizes human breast cancer cells to 5-Fluorouracil</title><author>Huang, Yanjing ; Yang, Shenghui ; Yu, Weiling ; Gui, Ling</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c326t-e2521b15da696be0bb2fcf564a08f2136997f4f185e604be4b124b29bda9c86a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>5-Fluorouracil</topic><topic>Antigens</topic><topic>Antigens, Nuclear</topic><topic>Apoptosis</topic><topic>Breast cancer</topic><topic>Breast Neoplasms - drug therapy</topic><topic>Cancer Research</topic><topic>Cell Line, Tumor</topic><topic>Cell Survival</topic><topic>Cell viability</topic><topic>Drug Resistance, Neoplasm</topic><topic>Evaluation</topic><topic>Fluorouracil - pharmacology</topic><topic>Gene expression</topic><topic>Humans</topic><topic>Immunoprecipitation</topic><topic>Isotypes</topic><topic>Male</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>mRNA</topic><topic>Oncology</topic><topic>Overexpression</topic><topic>Pharmacology/Toxicology</topic><topic>Polymerase chain reaction</topic><topic>Proteins</topic><topic>Sensitivity</topic><topic>Short Communication</topic><topic>Sperm</topic><topic>Spermatozoa</topic><topic>TRAF6 protein</topic><topic>Tumor necrosis factor</topic><topic>Tumor necrosis factor receptors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Huang, Yanjing</creatorcontrib><creatorcontrib>Yang, Shenghui</creatorcontrib><creatorcontrib>Yu, Weiling</creatorcontrib><creatorcontrib>Gui, Ling</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central</collection><collection>AUTh Library subscriptions: ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>MEDLINE - Academic</collection><jtitle>Cancer chemotherapy and pharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Huang, Yanjing</au><au>Yang, Shenghui</au><au>Yu, Weiling</au><au>Gui, Ling</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Somatic nuclear auto-antigenic sperm protein sensitizes human breast cancer cells to 5-Fluorouracil</atitle><jtitle>Cancer chemotherapy and pharmacology</jtitle><stitle>Cancer Chemother Pharmacol</stitle><addtitle>Cancer Chemother Pharmacol</addtitle><date>2022-04-01</date><risdate>2022</risdate><volume>89</volume><issue>4</issue><spage>559</spage><epage>564</epage><pages>559-564</pages><issn>0344-5704</issn><eissn>1432-0843</eissn><abstract>Purpose
To assess the potential role of nuclear auto-antigenic sperm protein (NASP) in the cellular sensitivity to 5-Fluorouracil (5-FU) in breast cancer cells.
Methods
The expression of two NASP isotypes, namely somatic NASP (sNASP) and testis NASP (tNASP) in breast cancer lines were detected under 5-FU treatment using real-time polymerase chain reaction and western blot assays. NASP effect on cellular viability and apoptosis under 5-FU treatment were evaluated. The interaction between NASP and its downstream proteins were evaluated using the co-immunoprecipitation (Co-IP) assays.
Results
5-FU significantly decreased the mRNA and protein expression levels of sNASP. Inhibition of sNASP increased cellular viability, colony formation ability, but reduced apoptosis in tested cell lines in response to 5-FU, which were reversed by sNASP over-expression. Further study reveals 5-FU disrupts sNASP/TNF receptor-associated factor 6 (TRAF6) complex, potentiates cellular sensitivity to 5-FU via NK-kB.
Conclusion
Our findings suggest sNASP is a novel molecular target having potential to overcome the resistance to 5-FU in breast cancer cells.</abstract><cop>Berlin/Heidelberg</cop><pub>Springer Berlin Heidelberg</pub><pmid>35133490</pmid><doi>10.1007/s00280-021-04391-2</doi><tpages>6</tpages><orcidid>https://orcid.org/0000-0001-5255-7589</orcidid></addata></record> |
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| subjects | 5-Fluorouracil Antigens Antigens, Nuclear Apoptosis Breast cancer Breast Neoplasms - drug therapy Cancer Research Cell Line, Tumor Cell Survival Cell viability Drug Resistance, Neoplasm Evaluation Fluorouracil - pharmacology Gene expression Humans Immunoprecipitation Isotypes Male Medicine Medicine & Public Health mRNA Oncology Overexpression Pharmacology/Toxicology Polymerase chain reaction Proteins Sensitivity Short Communication Sperm Spermatozoa TRAF6 protein Tumor necrosis factor Tumor necrosis factor receptors |
| title | Somatic nuclear auto-antigenic sperm protein sensitizes human breast cancer cells to 5-Fluorouracil |
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