MiR-203 is downregulated in laryngeal squamous cell carcinoma and can suppress proliferation and induce apoptosis of tumours
MicroRNAs (miRNAs) have been recognised to regulate cancer development and progression in carcinogenesis as either oncogenes or tumour suppressor genes. However, whether miR-203 plays a crucial role in human laryngeal squamous cell carcinoma (LSCC) remains largely unclear. In the study, we have foun...
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description | MicroRNAs (miRNAs) have been recognised to regulate cancer development and progression in carcinogenesis as either oncogenes or tumour suppressor genes. However, whether miR-203 plays a crucial role in human laryngeal squamous cell carcinoma (LSCC) remains largely unclear. In the study, we have found that miR-203 expression was significantly lower in LSCC tissues than that in corresponding adjacent non-neoplastic tissues and was negatively correlated with ASAP1 expression level. Lower expression of miR-203 was significantly related to poor differentiation, advanced clinical stages, T3–4 tumour grade, lymph node metastasis and decreased 5-year overall survival. Transfection with miR-203 inhibited proliferation, reduced invasion, induced apoptosis and caused G1 phase cell cycle arrest of Hep-2 cells in vitro, suggesting that miR-203 functioned as a tumour suppressor. We have also tested that over-expression of miR-203 may both suppress the growth of xenograft tumours in mice and downregulate the expressions of ASAP1 in vivo. Furthermore, miR-203 may regulate the expressions of mesenchymal transition (EMT) marker of E-cadherin and cancer stem cells (CSCs) marker of CD44. These findings suggest that miR-203 plays a role as a tumour suppressor in LSCC, likely by regulating ASAP1, probably in relation to EMT and CSCs and may serve as a potential target for therapeutic intervention. |
doi_str_mv | 10.1007/s13277-014-1790-7 |
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However, whether miR-203 plays a crucial role in human laryngeal squamous cell carcinoma (LSCC) remains largely unclear. In the study, we have found that miR-203 expression was significantly lower in LSCC tissues than that in corresponding adjacent non-neoplastic tissues and was negatively correlated with ASAP1 expression level. Lower expression of miR-203 was significantly related to poor differentiation, advanced clinical stages, T3–4 tumour grade, lymph node metastasis and decreased 5-year overall survival. Transfection with miR-203 inhibited proliferation, reduced invasion, induced apoptosis and caused G1 phase cell cycle arrest of Hep-2 cells in vitro, suggesting that miR-203 functioned as a tumour suppressor. We have also tested that over-expression of miR-203 may both suppress the growth of xenograft tumours in mice and downregulate the expressions of ASAP1 in vivo. Furthermore, miR-203 may regulate the expressions of mesenchymal transition (EMT) marker of E-cadherin and cancer stem cells (CSCs) marker of CD44. These findings suggest that miR-203 plays a role as a tumour suppressor in LSCC, likely by regulating ASAP1, probably in relation to EMT and CSCs and may serve as a potential target for therapeutic intervention.</description><identifier>ISSN: 1010-4283</identifier><identifier>EISSN: 1423-0380</identifier><identifier>DOI: 10.1007/s13277-014-1790-7</identifier><identifier>PMID: 24682952</identifier><language>eng</language><publisher>Dordrecht: Springer Netherlands</publisher><subject>Adaptor Proteins, Signal Transducing - analysis ; Adult ; Aged ; Animals ; Apoptosis ; Biomedical and Life Sciences ; Biomedicine ; Cadherins - analysis ; Cancer Research ; Carcinoma, Squamous Cell - pathology ; Cell Proliferation ; Cellular biology ; Down-Regulation ; Epithelial-Mesenchymal Transition ; Female ; Gene expression ; Genes, Tumor Suppressor - physiology ; Head and Neck Neoplasms - pathology ; Humans ; Hyaluronan Receptors - analysis ; Laryngeal cancer ; Laryngeal Neoplasms - pathology ; Male ; Mice ; Mice, Inbred BALB C ; MicroRNAs ; MicroRNAs - analysis ; MicroRNAs - physiology ; Middle Aged ; Neoplasm Invasiveness ; Research Article ; Squamous Cell Carcinoma of Head and Neck</subject><ispartof>Tumor biology, 2014-06, Vol.35 (6), p.5953-5963</ispartof><rights>International Society of Oncology and BioMarkers (ISOBM) 2014</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c442t-61b4ae2c6124cb80ee4fc306b395d020bbb2923b28929c4e4b0ceb20d20726d53</citedby><cites>FETCH-LOGICAL-c442t-61b4ae2c6124cb80ee4fc306b395d020bbb2923b28929c4e4b0ceb20d20726d53</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s13277-014-1790-7$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s13277-014-1790-7$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24682952$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Tian, Linli</creatorcontrib><creatorcontrib>Li, Minghua</creatorcontrib><creatorcontrib>Ge, Jingchun</creatorcontrib><creatorcontrib>Guo, Yan</creatorcontrib><creatorcontrib>Sun, Yanan</creatorcontrib><creatorcontrib>Liu, Ming</creatorcontrib><creatorcontrib>Xiao, Hui</creatorcontrib><title>MiR-203 is downregulated in laryngeal squamous cell carcinoma and can suppress proliferation and induce apoptosis of tumours</title><title>Tumor biology</title><addtitle>Tumor Biol</addtitle><addtitle>Tumour Biol</addtitle><description>MicroRNAs (miRNAs) have been recognised to regulate cancer development and progression in carcinogenesis as either oncogenes or tumour suppressor genes. However, whether miR-203 plays a crucial role in human laryngeal squamous cell carcinoma (LSCC) remains largely unclear. In the study, we have found that miR-203 expression was significantly lower in LSCC tissues than that in corresponding adjacent non-neoplastic tissues and was negatively correlated with ASAP1 expression level. Lower expression of miR-203 was significantly related to poor differentiation, advanced clinical stages, T3–4 tumour grade, lymph node metastasis and decreased 5-year overall survival. Transfection with miR-203 inhibited proliferation, reduced invasion, induced apoptosis and caused G1 phase cell cycle arrest of Hep-2 cells in vitro, suggesting that miR-203 functioned as a tumour suppressor. We have also tested that over-expression of miR-203 may both suppress the growth of xenograft tumours in mice and downregulate the expressions of ASAP1 in vivo. Furthermore, miR-203 may regulate the expressions of mesenchymal transition (EMT) marker of E-cadherin and cancer stem cells (CSCs) marker of CD44. These findings suggest that miR-203 plays a role as a tumour suppressor in LSCC, likely by regulating ASAP1, probably in relation to EMT and CSCs and may serve as a potential target for therapeutic intervention.</description><subject>Adaptor Proteins, Signal Transducing - analysis</subject><subject>Adult</subject><subject>Aged</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Cadherins - analysis</subject><subject>Cancer Research</subject><subject>Carcinoma, Squamous Cell - pathology</subject><subject>Cell Proliferation</subject><subject>Cellular biology</subject><subject>Down-Regulation</subject><subject>Epithelial-Mesenchymal Transition</subject><subject>Female</subject><subject>Gene expression</subject><subject>Genes, Tumor Suppressor - physiology</subject><subject>Head and Neck Neoplasms - pathology</subject><subject>Humans</subject><subject>Hyaluronan Receptors - analysis</subject><subject>Laryngeal cancer</subject><subject>Laryngeal Neoplasms - pathology</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>MicroRNAs</subject><subject>MicroRNAs - analysis</subject><subject>MicroRNAs - physiology</subject><subject>Middle Aged</subject><subject>Neoplasm Invasiveness</subject><subject>Research Article</subject><subject>Squamous Cell Carcinoma of Head and Neck</subject><issn>1010-4283</issn><issn>1423-0380</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>BENPR</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNp1kE9rHDEMxU1IySZpP0AuxdCzE1n2_PGxLG0TSAmE5Gxsj2eZZdaetWcohXz4Otlt6SUnSejpPfEj5IrDNQdobjIX2DQMuGS8UcCaE3LOJQoGooXT0gMHJrEVK3KR8xaAV0rVZ2SFsm5RVXhOXn4OjwxB0CHTLv4KyW-W0cy-o0Ogo0m_w8abkeb9YnZxydT5caTOJDeEuDPUhK5MgeZlmpLPmU4pjkPvk5mHGN7WQ-gW56mZ4jTHXGJiT-elmKX8kXzozZj9p2O9JM_fvz2tb9n9w4-79dd75qTEmdXcSuPR1Rylsy14L3snoLZCVR0gWGtRobDYKlROemnBeYvQITRYd5W4JF8OvuW7_eLzrLclPpRIzSshGxRK8aLiB5VLMefkez2lYVcQaA76lbc-8NaFt37lrZty8_novNid7_5d_AVcBHgQ5LIqLNN_0e-6_gG5g4xR</recordid><startdate>20140601</startdate><enddate>20140601</enddate><creator>Tian, Linli</creator><creator>Li, Minghua</creator><creator>Ge, Jingchun</creator><creator>Guo, Yan</creator><creator>Sun, Yanan</creator><creator>Liu, Ming</creator><creator>Xiao, Hui</creator><general>Springer Netherlands</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>7T5</scope><scope>7TO</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>M7P</scope><scope>MBDVC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope></search><sort><creationdate>20140601</creationdate><title>MiR-203 is downregulated in laryngeal squamous cell carcinoma and can suppress proliferation and induce apoptosis of tumours</title><author>Tian, Linli ; Li, Minghua ; Ge, Jingchun ; Guo, Yan ; Sun, Yanan ; Liu, Ming ; Xiao, Hui</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c442t-61b4ae2c6124cb80ee4fc306b395d020bbb2923b28929c4e4b0ceb20d20726d53</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>Adaptor Proteins, Signal Transducing - analysis</topic><topic>Adult</topic><topic>Aged</topic><topic>Animals</topic><topic>Apoptosis</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Cadherins - analysis</topic><topic>Cancer Research</topic><topic>Carcinoma, Squamous Cell - pathology</topic><topic>Cell Proliferation</topic><topic>Cellular biology</topic><topic>Down-Regulation</topic><topic>Epithelial-Mesenchymal Transition</topic><topic>Female</topic><topic>Gene expression</topic><topic>Genes, Tumor Suppressor - physiology</topic><topic>Head and Neck Neoplasms - pathology</topic><topic>Humans</topic><topic>Hyaluronan Receptors - analysis</topic><topic>Laryngeal cancer</topic><topic>Laryngeal Neoplasms - pathology</topic><topic>Male</topic><topic>Mice</topic><topic>Mice, Inbred BALB C</topic><topic>MicroRNAs</topic><topic>MicroRNAs - analysis</topic><topic>MicroRNAs - physiology</topic><topic>Middle Aged</topic><topic>Neoplasm Invasiveness</topic><topic>Research Article</topic><topic>Squamous Cell Carcinoma of Head and Neck</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Tian, Linli</creatorcontrib><creatorcontrib>Li, Minghua</creatorcontrib><creatorcontrib>Ge, Jingchun</creatorcontrib><creatorcontrib>Guo, Yan</creatorcontrib><creatorcontrib>Sun, Yanan</creatorcontrib><creatorcontrib>Liu, Ming</creatorcontrib><creatorcontrib>Xiao, Hui</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>Immunology Abstracts</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>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Biological Science Database</collection><collection>Research Library (Corporate)</collection><collection>Publicly Available Content 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>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><jtitle>Tumor biology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Tian, Linli</au><au>Li, Minghua</au><au>Ge, Jingchun</au><au>Guo, Yan</au><au>Sun, Yanan</au><au>Liu, Ming</au><au>Xiao, Hui</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>MiR-203 is downregulated in laryngeal squamous cell carcinoma and can suppress proliferation and induce apoptosis of tumours</atitle><jtitle>Tumor biology</jtitle><stitle>Tumor Biol</stitle><addtitle>Tumour Biol</addtitle><date>2014-06-01</date><risdate>2014</risdate><volume>35</volume><issue>6</issue><spage>5953</spage><epage>5963</epage><pages>5953-5963</pages><issn>1010-4283</issn><eissn>1423-0380</eissn><abstract>MicroRNAs (miRNAs) have been recognised to regulate cancer development and progression in carcinogenesis as either oncogenes or tumour suppressor genes. However, whether miR-203 plays a crucial role in human laryngeal squamous cell carcinoma (LSCC) remains largely unclear. In the study, we have found that miR-203 expression was significantly lower in LSCC tissues than that in corresponding adjacent non-neoplastic tissues and was negatively correlated with ASAP1 expression level. Lower expression of miR-203 was significantly related to poor differentiation, advanced clinical stages, T3–4 tumour grade, lymph node metastasis and decreased 5-year overall survival. Transfection with miR-203 inhibited proliferation, reduced invasion, induced apoptosis and caused G1 phase cell cycle arrest of Hep-2 cells in vitro, suggesting that miR-203 functioned as a tumour suppressor. We have also tested that over-expression of miR-203 may both suppress the growth of xenograft tumours in mice and downregulate the expressions of ASAP1 in vivo. Furthermore, miR-203 may regulate the expressions of mesenchymal transition (EMT) marker of E-cadherin and cancer stem cells (CSCs) marker of CD44. These findings suggest that miR-203 plays a role as a tumour suppressor in LSCC, likely by regulating ASAP1, probably in relation to EMT and CSCs and may serve as a potential target for therapeutic intervention.</abstract><cop>Dordrecht</cop><pub>Springer Netherlands</pub><pmid>24682952</pmid><doi>10.1007/s13277-014-1790-7</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Adaptor Proteins, Signal Transducing - analysis Adult Aged Animals Apoptosis Biomedical and Life Sciences Biomedicine Cadherins - analysis Cancer Research Carcinoma, Squamous Cell - pathology Cell Proliferation Cellular biology Down-Regulation Epithelial-Mesenchymal Transition Female Gene expression Genes, Tumor Suppressor - physiology Head and Neck Neoplasms - pathology Humans Hyaluronan Receptors - analysis Laryngeal cancer Laryngeal Neoplasms - pathology Male Mice Mice, Inbred BALB C MicroRNAs MicroRNAs - analysis MicroRNAs - physiology Middle Aged Neoplasm Invasiveness Research Article Squamous Cell Carcinoma of Head and Neck |
title | MiR-203 is downregulated in laryngeal squamous cell carcinoma and can suppress proliferation and induce apoptosis of tumours |
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