Reciprocal expression of Slug and Snail in human oral cancer cells
Snail, also called Snai1, is a key regulator of EMT. Snail plays crucial roles in cancer progression, including resistance to anti-tumor drugs and invasion by various cancer cells. Slug, also known as Snai2, is also involved in the aggravation of certain tumors. In this study, we examined the roles...
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| creator | Nakamura, Ryosuke Ishii, Hiroki Endo, Kaori Hotta, Asami Fujii, Eiji Miyazawa, Keiji Saitoh, Masao |
| description | Snail, also called Snai1, is a key regulator of EMT. Snail plays crucial roles in cancer progression, including resistance to anti-tumor drugs and invasion by various cancer cells. Slug, also known as Snai2, is also involved in the aggravation of certain tumors. In this study, we examined the roles of Slug in human oral squamous cell carcinoma (OSCC) cells. Slug is highly expressed in these cells, and Slug siRNA effectively represses anti-tumor drug resistance and invasive properties. In addition, transforming growth factor (TGF)-β upregulates the expression of Snail and Slug and promotes resistance to anti-tumor drugs in OSCC cells. Surprisingly, Slug siRNA appears to upregulate Snail expression considerably in OSCC cells. Snail siRNA also appears to upregulate Slug expression. Thus, either Slug or Snail siRNA alone partially mitigates malignant phenotypes in the presence of TGF-β, whereas both Slug and Snail siRNAs together dramatically suppress them. Therefore, Slug and Snail in tandem, but not alone, are potential therapeutic targets for nucleic acid medicines to treat oral cancer. |
| doi_str_mv | 10.1371/journal.pone.0199442 |
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Snail plays crucial roles in cancer progression, including resistance to anti-tumor drugs and invasion by various cancer cells. Slug, also known as Snai2, is also involved in the aggravation of certain tumors. In this study, we examined the roles of Slug in human oral squamous cell carcinoma (OSCC) cells. Slug is highly expressed in these cells, and Slug siRNA effectively represses anti-tumor drug resistance and invasive properties. In addition, transforming growth factor (TGF)-β upregulates the expression of Snail and Slug and promotes resistance to anti-tumor drugs in OSCC cells. Surprisingly, Slug siRNA appears to upregulate Snail expression considerably in OSCC cells. Snail siRNA also appears to upregulate Slug expression. Thus, either Slug or Snail siRNA alone partially mitigates malignant phenotypes in the presence of TGF-β, whereas both Slug and Snail siRNAs together dramatically suppress them. Therefore, Slug and Snail in tandem, but not alone, are potential therapeutic targets for nucleic acid medicines to treat oral cancer.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0199442</identifier><identifier>PMID: 29969465</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Antineoplastic Agents - pharmacology ; Apoptosis ; Biochemistry ; Biology and life sciences ; Biomarkers ; Breast cancer ; Cancer ; Care and treatment ; Cell adhesion & migration ; Cell cycle ; Cell Line, Tumor ; Cytokines - genetics ; Cytokines - metabolism ; Development and progression ; Drug development ; Drug resistance ; Drug Resistance, Neoplasm - drug effects ; Drug Resistance, Neoplasm - genetics ; Drugs ; Epithelial-Mesenchymal Transition - drug effects ; Epithelial-Mesenchymal Transition - genetics ; Gene Expression Regulation, Neoplastic - drug effects ; Genetic aspects ; Growth factors ; Health education ; Humans ; Interdisciplinary aspects ; Invasiveness ; Kinases ; Maxillofacial surgery ; Medicine ; Medicine and Health Sciences ; Metastasis ; Motility ; Mouth cancer ; Mouth Neoplasms - genetics ; Mouth Neoplasms - metabolism ; Mouth Neoplasms - pathology ; Nakamura, Hiroki ; Oral cancer ; Oral squamous cell carcinoma ; Phenotypes ; Proteins ; Research and Analysis Methods ; siRNA ; Snail Family Transcription Factors - genetics ; Snail Family Transcription Factors - metabolism ; Snail protein ; Snails ; Squamous cell carcinoma ; Surgery ; Therapeutic applications ; Transcription factors ; Transforming growth factor ; Transforming Growth Factor beta - metabolism ; Transforming Growth Factor beta - pharmacology ; Transforming growth factors ; Tumors</subject><ispartof>PloS one, 2018-07, Vol.13 (7), p.e0199442-e0199442</ispartof><rights>COPYRIGHT 2018 Public Library of Science</rights><rights>2018 Nakamura 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. 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Snail plays crucial roles in cancer progression, including resistance to anti-tumor drugs and invasion by various cancer cells. Slug, also known as Snai2, is also involved in the aggravation of certain tumors. In this study, we examined the roles of Slug in human oral squamous cell carcinoma (OSCC) cells. Slug is highly expressed in these cells, and Slug siRNA effectively represses anti-tumor drug resistance and invasive properties. In addition, transforming growth factor (TGF)-β upregulates the expression of Snail and Slug and promotes resistance to anti-tumor drugs in OSCC cells. Surprisingly, Slug siRNA appears to upregulate Snail expression considerably in OSCC cells. Snail siRNA also appears to upregulate Slug expression. Thus, either Slug or Snail siRNA alone partially mitigates malignant phenotypes in the presence of TGF-β, whereas both Slug and Snail siRNAs together dramatically suppress them. Therefore, Slug and Snail in tandem, but not alone, are potential therapeutic targets for nucleic acid medicines to treat oral cancer.</description><subject>Antineoplastic Agents - pharmacology</subject><subject>Apoptosis</subject><subject>Biochemistry</subject><subject>Biology and life sciences</subject><subject>Biomarkers</subject><subject>Breast cancer</subject><subject>Cancer</subject><subject>Care and treatment</subject><subject>Cell adhesion & migration</subject><subject>Cell cycle</subject><subject>Cell Line, Tumor</subject><subject>Cytokines - genetics</subject><subject>Cytokines - metabolism</subject><subject>Development and progression</subject><subject>Drug development</subject><subject>Drug resistance</subject><subject>Drug Resistance, Neoplasm - drug effects</subject><subject>Drug Resistance, Neoplasm - genetics</subject><subject>Drugs</subject><subject>Epithelial-Mesenchymal Transition - drug effects</subject><subject>Epithelial-Mesenchymal Transition - genetics</subject><subject>Gene Expression Regulation, Neoplastic - 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Snail plays crucial roles in cancer progression, including resistance to anti-tumor drugs and invasion by various cancer cells. Slug, also known as Snai2, is also involved in the aggravation of certain tumors. In this study, we examined the roles of Slug in human oral squamous cell carcinoma (OSCC) cells. Slug is highly expressed in these cells, and Slug siRNA effectively represses anti-tumor drug resistance and invasive properties. In addition, transforming growth factor (TGF)-β upregulates the expression of Snail and Slug and promotes resistance to anti-tumor drugs in OSCC cells. Surprisingly, Slug siRNA appears to upregulate Snail expression considerably in OSCC cells. Snail siRNA also appears to upregulate Slug expression. Thus, either Slug or Snail siRNA alone partially mitigates malignant phenotypes in the presence of TGF-β, whereas both Slug and Snail siRNAs together dramatically suppress them. Therefore, Slug and Snail in tandem, but not alone, are potential therapeutic targets for nucleic acid medicines to treat oral cancer.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>29969465</pmid><doi>10.1371/journal.pone.0199442</doi><tpages>e0199442</tpages><orcidid>https://orcid.org/0000-0003-1329-2180</orcidid><orcidid>https://orcid.org/0000-0003-0793-1679</orcidid><oa>free_for_read</oa></addata></record> |
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| ispartof | PloS one, 2018-07, Vol.13 (7), p.e0199442-e0199442 |
| issn | 1932-6203 1932-6203 |
| language | eng |
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| source | MEDLINE; DOAJ Directory of Open Access Journals; Public Library of Science (PLoS); EZB-FREE-00999 freely available EZB journals; PubMed Central; Free Full-Text Journals in Chemistry |
| subjects | Antineoplastic Agents - pharmacology Apoptosis Biochemistry Biology and life sciences Biomarkers Breast cancer Cancer Care and treatment Cell adhesion & migration Cell cycle Cell Line, Tumor Cytokines - genetics Cytokines - metabolism Development and progression Drug development Drug resistance Drug Resistance, Neoplasm - drug effects Drug Resistance, Neoplasm - genetics Drugs Epithelial-Mesenchymal Transition - drug effects Epithelial-Mesenchymal Transition - genetics Gene Expression Regulation, Neoplastic - drug effects Genetic aspects Growth factors Health education Humans Interdisciplinary aspects Invasiveness Kinases Maxillofacial surgery Medicine Medicine and Health Sciences Metastasis Motility Mouth cancer Mouth Neoplasms - genetics Mouth Neoplasms - metabolism Mouth Neoplasms - pathology Nakamura, Hiroki Oral cancer Oral squamous cell carcinoma Phenotypes Proteins Research and Analysis Methods siRNA Snail Family Transcription Factors - genetics Snail Family Transcription Factors - metabolism Snail protein Snails Squamous cell carcinoma Surgery Therapeutic applications Transcription factors Transforming growth factor Transforming Growth Factor beta - metabolism Transforming Growth Factor beta - pharmacology Transforming growth factors Tumors |
| title | Reciprocal expression of Slug and Snail in human oral cancer cells |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-06T02%3A38%3A48IST&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=Reciprocal%20expression%20of%20Slug%20and%20Snail%20in%20human%20oral%20cancer%20cells&rft.jtitle=PloS%20one&rft.au=Nakamura,%20Ryosuke&rft.date=2018-07-03&rft.volume=13&rft.issue=7&rft.spage=e0199442&rft.epage=e0199442&rft.pages=e0199442-e0199442&rft.issn=1932-6203&rft.eissn=1932-6203&rft_id=info:doi/10.1371/journal.pone.0199442&rft_dat=%3Cgale_plos_%3EA547840743%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=2063686044&rft_id=info:pmid/29969465&rft_galeid=A547840743&rft_doaj_id=oai_doaj_org_article_7caf16414c254e5ab3467dbe0fc4f3e8&rfr_iscdi=true |