Expression of Cell Competition Markers at the Interface between p53 Signature and Normal Epithelium in the Human Fallopian Tube
There is a growing body of evidence regarding cell competition between normal and mutant mammalian cells, which suggest that it may play a defensive role in the early phase of carcinogenesis. In vitro study in the past has shown that overexpression of vimentin in normal epithelial cells at the conta...
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description | There is a growing body of evidence regarding cell competition between normal and mutant mammalian cells, which suggest that it may play a defensive role in the early phase of carcinogenesis. In vitro study in the past has shown that overexpression of vimentin in normal epithelial cells at the contact surface with transformed cells is essential for the cell competition involved in epithelial defense against cancer. In this study, we attempted to examine cell competition in human tissue in vivo by investigating surgically resected human fallopian tubes that contain p53 signatures and serous tubal intraepithelial lesions (STILs), a linear expansion of p53-immunopositive/TP53 mutant tubal epithelial cells that are considered as precursors of pelvic high grade serous carcinoma. Immunofluorescence double staining for p53 and the cell competition marker vimentin was performed in 21 sections of human fallopian tube tissue containing 17 p53 signatures and 4 STILs. The intensities of vimentin expression at the interface between p53-positive cells at the end of the p53 signature/STIL and adjacent p53-negative normal tubal epithelial cells were compared with the background tubal epithelium. As a result, the average vimentin intensity at the interfaces relative to the background intensity was 1.076 (95% CI, 0.9412 - 1.211 for p53 signature and 0.9790 (95% CI, 0.7206 - 1.237) for STIL. Thus, it can be concluded that overexpression of the cell competition marker vimentin are not observed in human tissue with TP53 alterations. |
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In vitro study in the past has shown that overexpression of vimentin in normal epithelial cells at the contact surface with transformed cells is essential for the cell competition involved in epithelial defense against cancer. In this study, we attempted to examine cell competition in human tissue in vivo by investigating surgically resected human fallopian tubes that contain p53 signatures and serous tubal intraepithelial lesions (STILs), a linear expansion of p53-immunopositive/TP53 mutant tubal epithelial cells that are considered as precursors of pelvic high grade serous carcinoma. Immunofluorescence double staining for p53 and the cell competition marker vimentin was performed in 21 sections of human fallopian tube tissue containing 17 p53 signatures and 4 STILs. The intensities of vimentin expression at the interface between p53-positive cells at the end of the p53 signature/STIL and adjacent p53-negative normal tubal epithelial cells were compared with the background tubal epithelium. As a result, the average vimentin intensity at the interfaces relative to the background intensity was 1.076 (95% CI, 0.9412 - 1.211 for p53 signature and 0.9790 (95% CI, 0.7206 - 1.237) for STIL. Thus, it can be concluded that overexpression of the cell competition marker vimentin are not observed in human tissue with TP53 alterations.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0156069</identifier><identifier>PMID: 27258067</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Adult ; Aged ; Algorithms ; Antigens ; Biological markers ; Biology and Life Sciences ; Biomarkers, Tumor - metabolism ; Carcinogenesis ; Carcinogens ; Cloning ; Competition ; Cystadenocarcinoma, Serous - metabolism ; Cystadenocarcinoma, Serous - pathology ; Drosophila ; Epithelial cells ; Epithelium ; Epithelium - metabolism ; Fallopian tube ; Fallopian Tube Neoplasms - metabolism ; Fallopian Tube Neoplasms - pathology ; Fallopian tubes ; Fallopian Tubes - metabolism ; Female ; Gynecology ; Humans ; Immunofluorescence ; In vivo methods and tests ; Influence ; Insects ; Interfaces ; Intermediate filament proteins ; Lesions ; Mammalian cells ; Medicine ; Medicine and Health Sciences ; Middle Aged ; Morphology ; Obstetrics ; Ovarian cancer ; p53 Protein ; Pathology ; Research and Analysis Methods ; Signatures ; Transformed cells ; Tubes ; Tumor Suppressor Protein p53 - metabolism ; Vimentin ; Vimentin - metabolism</subject><ispartof>PloS one, 2016-06, Vol.11 (6), p.e0156069</ispartof><rights>COPYRIGHT 2016 Public Library of Science</rights><rights>2016 Kito et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2016 Kito et al 2016 Kito et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c784t-974530295957dd0c2111fd4db72f391d7cf3f3b60fa6b408111bc1a324bad4ed3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4892575/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4892575/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,2096,2915,23845,27901,27902,53766,53768,79342,79343</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27258067$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kito, Masahiko</creatorcontrib><creatorcontrib>Maeda, Daichi</creatorcontrib><creatorcontrib>Kudo-Asabe, Yukitsugu</creatorcontrib><creatorcontrib>Sato, Naoki</creatorcontrib><creatorcontrib>Shih, Ie-Ming</creatorcontrib><creatorcontrib>Wang, Tian-Li</creatorcontrib><creatorcontrib>Tanaka, Masamitsu</creatorcontrib><creatorcontrib>Terada, Yukihiro</creatorcontrib><creatorcontrib>Goto, Akiteru</creatorcontrib><title>Expression of Cell Competition Markers at the Interface between p53 Signature and Normal Epithelium in the Human Fallopian Tube</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>There is a growing body of evidence regarding cell competition between normal and mutant mammalian cells, which suggest that it may play a defensive role in the early phase of carcinogenesis. In vitro study in the past has shown that overexpression of vimentin in normal epithelial cells at the contact surface with transformed cells is essential for the cell competition involved in epithelial defense against cancer. In this study, we attempted to examine cell competition in human tissue in vivo by investigating surgically resected human fallopian tubes that contain p53 signatures and serous tubal intraepithelial lesions (STILs), a linear expansion of p53-immunopositive/TP53 mutant tubal epithelial cells that are considered as precursors of pelvic high grade serous carcinoma. Immunofluorescence double staining for p53 and the cell competition marker vimentin was performed in 21 sections of human fallopian tube tissue containing 17 p53 signatures and 4 STILs. The intensities of vimentin expression at the interface between p53-positive cells at the end of the p53 signature/STIL and adjacent p53-negative normal tubal epithelial cells were compared with the background tubal epithelium. As a result, the average vimentin intensity at the interfaces relative to the background intensity was 1.076 (95% CI, 0.9412 - 1.211 for p53 signature and 0.9790 (95% CI, 0.7206 - 1.237) for STIL. Thus, it can be concluded that overexpression of the cell competition marker vimentin are not observed in human tissue with TP53 alterations.</description><subject>Adult</subject><subject>Aged</subject><subject>Algorithms</subject><subject>Antigens</subject><subject>Biological markers</subject><subject>Biology and Life Sciences</subject><subject>Biomarkers, Tumor - metabolism</subject><subject>Carcinogenesis</subject><subject>Carcinogens</subject><subject>Cloning</subject><subject>Competition</subject><subject>Cystadenocarcinoma, Serous - metabolism</subject><subject>Cystadenocarcinoma, Serous - pathology</subject><subject>Drosophila</subject><subject>Epithelial cells</subject><subject>Epithelium</subject><subject>Epithelium - metabolism</subject><subject>Fallopian tube</subject><subject>Fallopian Tube Neoplasms - metabolism</subject><subject>Fallopian Tube Neoplasms - pathology</subject><subject>Fallopian tubes</subject><subject>Fallopian Tubes - metabolism</subject><subject>Female</subject><subject>Gynecology</subject><subject>Humans</subject><subject>Immunofluorescence</subject><subject>In vivo methods and tests</subject><subject>Influence</subject><subject>Insects</subject><subject>Interfaces</subject><subject>Intermediate filament proteins</subject><subject>Lesions</subject><subject>Mammalian cells</subject><subject>Medicine</subject><subject>Medicine and Health Sciences</subject><subject>Middle Aged</subject><subject>Morphology</subject><subject>Obstetrics</subject><subject>Ovarian cancer</subject><subject>p53 Protein</subject><subject>Pathology</subject><subject>Research and Analysis Methods</subject><subject>Signatures</subject><subject>Transformed cells</subject><subject>Tubes</subject><subject>Tumor Suppressor Protein p53 - 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metabolism</topic><topic>Carcinogenesis</topic><topic>Carcinogens</topic><topic>Cloning</topic><topic>Competition</topic><topic>Cystadenocarcinoma, Serous - metabolism</topic><topic>Cystadenocarcinoma, Serous - pathology</topic><topic>Drosophila</topic><topic>Epithelial cells</topic><topic>Epithelium</topic><topic>Epithelium - metabolism</topic><topic>Fallopian tube</topic><topic>Fallopian Tube Neoplasms - metabolism</topic><topic>Fallopian Tube Neoplasms - pathology</topic><topic>Fallopian tubes</topic><topic>Fallopian Tubes - metabolism</topic><topic>Female</topic><topic>Gynecology</topic><topic>Humans</topic><topic>Immunofluorescence</topic><topic>In vivo methods and tests</topic><topic>Influence</topic><topic>Insects</topic><topic>Interfaces</topic><topic>Intermediate filament proteins</topic><topic>Lesions</topic><topic>Mammalian cells</topic><topic>Medicine</topic><topic>Medicine and Health Sciences</topic><topic>Middle Aged</topic><topic>Morphology</topic><topic>Obstetrics</topic><topic>Ovarian cancer</topic><topic>p53 Protein</topic><topic>Pathology</topic><topic>Research and Analysis Methods</topic><topic>Signatures</topic><topic>Transformed cells</topic><topic>Tubes</topic><topic>Tumor Suppressor Protein p53 - 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In vitro study in the past has shown that overexpression of vimentin in normal epithelial cells at the contact surface with transformed cells is essential for the cell competition involved in epithelial defense against cancer. In this study, we attempted to examine cell competition in human tissue in vivo by investigating surgically resected human fallopian tubes that contain p53 signatures and serous tubal intraepithelial lesions (STILs), a linear expansion of p53-immunopositive/TP53 mutant tubal epithelial cells that are considered as precursors of pelvic high grade serous carcinoma. Immunofluorescence double staining for p53 and the cell competition marker vimentin was performed in 21 sections of human fallopian tube tissue containing 17 p53 signatures and 4 STILs. The intensities of vimentin expression at the interface between p53-positive cells at the end of the p53 signature/STIL and adjacent p53-negative normal tubal epithelial cells were compared with the background tubal epithelium. As a result, the average vimentin intensity at the interfaces relative to the background intensity was 1.076 (95% CI, 0.9412 - 1.211 for p53 signature and 0.9790 (95% CI, 0.7206 - 1.237) for STIL. Thus, it can be concluded that overexpression of the cell competition marker vimentin are not observed in human tissue with TP53 alterations.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>27258067</pmid><doi>10.1371/journal.pone.0156069</doi><oa>free_for_read</oa></addata></record> |
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subjects | Adult Aged Algorithms Antigens Biological markers Biology and Life Sciences Biomarkers, Tumor - metabolism Carcinogenesis Carcinogens Cloning Competition Cystadenocarcinoma, Serous - metabolism Cystadenocarcinoma, Serous - pathology Drosophila Epithelial cells Epithelium Epithelium - metabolism Fallopian tube Fallopian Tube Neoplasms - metabolism Fallopian Tube Neoplasms - pathology Fallopian tubes Fallopian Tubes - metabolism Female Gynecology Humans Immunofluorescence In vivo methods and tests Influence Insects Interfaces Intermediate filament proteins Lesions Mammalian cells Medicine Medicine and Health Sciences Middle Aged Morphology Obstetrics Ovarian cancer p53 Protein Pathology Research and Analysis Methods Signatures Transformed cells Tubes Tumor Suppressor Protein p53 - metabolism Vimentin Vimentin - metabolism |
title | Expression of Cell Competition Markers at the Interface between p53 Signature and Normal Epithelium in the Human Fallopian Tube |
url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-10T16%3A51%3A38IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_plos_&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Expression%20of%20Cell%20Competition%20Markers%20at%20the%20Interface%20between%20p53%20Signature%20and%20Normal%20Epithelium%20in%20the%20Human%20Fallopian%20Tube&rft.jtitle=PloS%20one&rft.au=Kito,%20Masahiko&rft.date=2016-06-03&rft.volume=11&rft.issue=6&rft.spage=e0156069&rft.pages=e0156069-&rft.issn=1932-6203&rft.eissn=1932-6203&rft_id=info:doi/10.1371/journal.pone.0156069&rft_dat=%3Cgale_plos_%3EA454205542%3C/gale_plos_%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1793753236&rft_id=info:pmid/27258067&rft_galeid=A454205542&rft_doaj_id=oai_doaj_org_article_fe9254d1f48547eb88cfdda18b390b22&rfr_iscdi=true |