c-Myc promotes tumor proliferation and anti‑apoptosis by repressing p21 in rhabdomyosarcomas
v-myc avian myelocytomatosis viral oncogene homolog (c-Myc) is an important member protein of the Myc family that is important in cell cycle progression, apoptosis and tumorigenesis. In the present study, the role of c‑Myc in rhabdomyosarcoma (RMS) was assessed. Firstly, expression of endogenous c‑M...
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| Veröffentlicht in: | Molecular medicine reports 2017-10, Vol.16 (4), p.4089-4094 |
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| creator | Zhang, Jinghang Song, Na Zang, Dan Yu, Jian Li, Jinsong Di, Wenyu Guo, Ruina Zhao, Weixing Wang, Haijun |
| description | v-myc avian myelocytomatosis viral oncogene homolog (c-Myc) is an important member protein of the Myc family that is important in cell cycle progression, apoptosis and tumorigenesis. In the present study, the role of c‑Myc in rhabdomyosarcoma (RMS) was assessed. Firstly, expression of endogenous c‑Myc and cyclin dependent kinase inhibitor 1A (p21) was examined in normal skeletal muscle, RMS specimens and TE671 RMS cells by immunohistochemistry, reverse transcription‑quantitative polymerase chain reaction and western blotting. Furthermore, cell cycle progression and apoptosis were assessed in TE671 RMS cells following treatment with a c‑Myc inhibitor, 10058‑F4. The results demonstrated that c‑Myc was overexpressed in clinical RMS tissues and TE671 cells, with the highest expression observed in the most RMS samples. Expression of p21 protein and apoptosis function were increased following treatment with 10058‑F4, but no difference was observed in cell cycle progression. In conclusion, the present study indicated that c‑Myc promotes RMS development by inhibiting apoptosis through repression of p21 transcription. Further studies will be required to evaluate c‑Myc as a target for RMS clinical treatment. |
| doi_str_mv | 10.3892/mmr.2017.7101 |
| format | Article |
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In the present study, the role of c‑Myc in rhabdomyosarcoma (RMS) was assessed. Firstly, expression of endogenous c‑Myc and cyclin dependent kinase inhibitor 1A (p21) was examined in normal skeletal muscle, RMS specimens and TE671 RMS cells by immunohistochemistry, reverse transcription‑quantitative polymerase chain reaction and western blotting. Furthermore, cell cycle progression and apoptosis were assessed in TE671 RMS cells following treatment with a c‑Myc inhibitor, 10058‑F4. The results demonstrated that c‑Myc was overexpressed in clinical RMS tissues and TE671 cells, with the highest expression observed in the most RMS samples. Expression of p21 protein and apoptosis function were increased following treatment with 10058‑F4, but no difference was observed in cell cycle progression. In conclusion, the present study indicated that c‑Myc promotes RMS development by inhibiting apoptosis through repression of p21 transcription. Further studies will be required to evaluate c‑Myc as a target for RMS clinical treatment.</description><identifier>ISSN: 1791-2997</identifier><identifier>EISSN: 1791-3004</identifier><identifier>DOI: 10.3892/mmr.2017.7101</identifier><identifier>PMID: 28765944</identifier><language>eng</language><publisher>Greece: Spandidos Publications</publisher><subject>Adolescent ; Aged ; Apoptosis ; Biotechnology ; c-Myc protein ; Cancer ; Carcinogenesis - genetics ; Carcinogenesis - pathology ; Care and treatment ; Cell cycle ; Cell Cycle - genetics ; Cell growth ; Cell Line, Tumor ; Cell Proliferation ; Child ; Child, Preschool ; Cyclin-dependent kinase inhibitor p21 ; Cyclin-Dependent Kinase Inhibitor p21 - genetics ; Cyclin-Dependent Kinase Inhibitor p21 - metabolism ; Cyclin-dependent kinases ; Development and progression ; Enzyme inhibitors ; Female ; Gene expression ; Gene Expression Regulation, Neoplastic - drug effects ; Gene silencing ; Genetic aspects ; GTP-binding protein ; Health aspects ; Humans ; Immunohistochemistry ; Kinases ; Male ; Middle Aged ; Musculoskeletal system ; Myc protein ; Oncogenes ; Polymerase chain reaction ; Proteins ; Proto-Oncogene Proteins c-myc - metabolism ; Reverse transcription ; Rhabdomyosarcoma ; Rhabdomyosarcoma - genetics ; Rhabdomyosarcoma - metabolism ; Rhabdomyosarcoma - pathology ; RNA, Messenger - genetics ; RNA, Messenger - metabolism ; Skeletal muscle ; Thiazoles - pharmacology ; Transcription, Genetic - drug effects ; Tumorigenesis ; Tumors ; Western blotting ; Young Adult</subject><ispartof>Molecular medicine reports, 2017-10, Vol.16 (4), p.4089-4094</ispartof><rights>COPYRIGHT 2017 Spandidos Publications</rights><rights>Copyright Spandidos Publications UK Ltd. 2017</rights><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c427t-66a218398e761f02b89df277ae3150078b9cfd3167f3ffbb4bf1ddec10b4b32f3</citedby><cites>FETCH-LOGICAL-c427t-66a218398e761f02b89df277ae3150078b9cfd3167f3ffbb4bf1ddec10b4b32f3</cites></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/28765944$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhang, Jinghang</creatorcontrib><creatorcontrib>Song, Na</creatorcontrib><creatorcontrib>Zang, Dan</creatorcontrib><creatorcontrib>Yu, Jian</creatorcontrib><creatorcontrib>Li, Jinsong</creatorcontrib><creatorcontrib>Di, Wenyu</creatorcontrib><creatorcontrib>Guo, Ruina</creatorcontrib><creatorcontrib>Zhao, Weixing</creatorcontrib><creatorcontrib>Wang, Haijun</creatorcontrib><title>c-Myc promotes tumor proliferation and anti‑apoptosis by repressing p21 in rhabdomyosarcomas</title><title>Molecular medicine reports</title><addtitle>Mol Med Rep</addtitle><description>v-myc avian myelocytomatosis viral oncogene homolog (c-Myc) is an important member protein of the Myc family that is important in cell cycle progression, apoptosis and tumorigenesis. In the present study, the role of c‑Myc in rhabdomyosarcoma (RMS) was assessed. Firstly, expression of endogenous c‑Myc and cyclin dependent kinase inhibitor 1A (p21) was examined in normal skeletal muscle, RMS specimens and TE671 RMS cells by immunohistochemistry, reverse transcription‑quantitative polymerase chain reaction and western blotting. Furthermore, cell cycle progression and apoptosis were assessed in TE671 RMS cells following treatment with a c‑Myc inhibitor, 10058‑F4. The results demonstrated that c‑Myc was overexpressed in clinical RMS tissues and TE671 cells, with the highest expression observed in the most RMS samples. Expression of p21 protein and apoptosis function were increased following treatment with 10058‑F4, but no difference was observed in cell cycle progression. In conclusion, the present study indicated that c‑Myc promotes RMS development by inhibiting apoptosis through repression of p21 transcription. Further studies will be required to evaluate c‑Myc as a target for RMS clinical treatment.</description><subject>Adolescent</subject><subject>Aged</subject><subject>Apoptosis</subject><subject>Biotechnology</subject><subject>c-Myc protein</subject><subject>Cancer</subject><subject>Carcinogenesis - genetics</subject><subject>Carcinogenesis - pathology</subject><subject>Care and treatment</subject><subject>Cell cycle</subject><subject>Cell Cycle - genetics</subject><subject>Cell growth</subject><subject>Cell Line, Tumor</subject><subject>Cell Proliferation</subject><subject>Child</subject><subject>Child, Preschool</subject><subject>Cyclin-dependent kinase inhibitor p21</subject><subject>Cyclin-Dependent Kinase Inhibitor p21 - genetics</subject><subject>Cyclin-Dependent Kinase Inhibitor p21 - metabolism</subject><subject>Cyclin-dependent kinases</subject><subject>Development and progression</subject><subject>Enzyme inhibitors</subject><subject>Female</subject><subject>Gene expression</subject><subject>Gene Expression Regulation, Neoplastic - drug effects</subject><subject>Gene silencing</subject><subject>Genetic aspects</subject><subject>GTP-binding protein</subject><subject>Health aspects</subject><subject>Humans</subject><subject>Immunohistochemistry</subject><subject>Kinases</subject><subject>Male</subject><subject>Middle Aged</subject><subject>Musculoskeletal system</subject><subject>Myc protein</subject><subject>Oncogenes</subject><subject>Polymerase chain reaction</subject><subject>Proteins</subject><subject>Proto-Oncogene Proteins c-myc - metabolism</subject><subject>Reverse transcription</subject><subject>Rhabdomyosarcoma</subject><subject>Rhabdomyosarcoma - genetics</subject><subject>Rhabdomyosarcoma - metabolism</subject><subject>Rhabdomyosarcoma - pathology</subject><subject>RNA, Messenger - genetics</subject><subject>RNA, Messenger - metabolism</subject><subject>Skeletal muscle</subject><subject>Thiazoles - pharmacology</subject><subject>Transcription, Genetic - drug effects</subject><subject>Tumorigenesis</subject><subject>Tumors</subject><subject>Western blotting</subject><subject>Young Adult</subject><issn>1791-2997</issn><issn>1791-3004</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNptkc9OHSEUh4mxUasu3TaTuOlmbjkwDLA0pv8STTftVsIwoJhhmMLM4u76Cr6iTyITr5o2DSEcyHcOv-RD6AzwhgpJPoWQNgQD33DAsIeOgEuoKcbN_q4mUvJD9D7ne4xbRpg8QIdE8JbJpjlCN6a-3ppqSjHE2eZqXkJM63XwziY9-zhWeuzLnv3jnwc9xWmO2eeq21bJTsnm7MfbaiJQ-bFKd7rrY9jGrJOJQecT9M7pIdvT3XmMfn35_PPyW3314-v3y4ur2jSEz3XbagKCSmF5Cw6TTsjeEc61pcAw5qKTxvUUWu6oc13XdA763hrApaTE0WP08XluSf57sXlWwWdjh0GPNi5ZgSSMQYM5Luj5P-h9XNJY0hVKlM8YkeKNutWDVX50cU7arEPVBaNABOO4LdTmP1RZvQ3exNE6X97_aqifG0yKOSfr1JR80GmrAKvVpyo-1epTrT4L_2EXdumC7V_pF4H0CQWVm5w</recordid><startdate>20171001</startdate><enddate>20171001</enddate><creator>Zhang, Jinghang</creator><creator>Song, Na</creator><creator>Zang, Dan</creator><creator>Yu, Jian</creator><creator>Li, Jinsong</creator><creator>Di, Wenyu</creator><creator>Guo, Ruina</creator><creator>Zhao, Weixing</creator><creator>Wang, Haijun</creator><general>Spandidos Publications</general><general>Spandidos Publications UK Ltd</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>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AN0</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>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope></search><sort><creationdate>20171001</creationdate><title>c-Myc promotes tumor proliferation and anti‑apoptosis by repressing p21 in rhabdomyosarcomas</title><author>Zhang, Jinghang ; Song, Na ; Zang, Dan ; Yu, Jian ; Li, Jinsong ; Di, Wenyu ; Guo, Ruina ; Zhao, Weixing ; Wang, Haijun</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c427t-66a218398e761f02b89df277ae3150078b9cfd3167f3ffbb4bf1ddec10b4b32f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Adolescent</topic><topic>Aged</topic><topic>Apoptosis</topic><topic>Biotechnology</topic><topic>c-Myc protein</topic><topic>Cancer</topic><topic>Carcinogenesis - genetics</topic><topic>Carcinogenesis - pathology</topic><topic>Care and treatment</topic><topic>Cell cycle</topic><topic>Cell Cycle - genetics</topic><topic>Cell growth</topic><topic>Cell Line, Tumor</topic><topic>Cell Proliferation</topic><topic>Child</topic><topic>Child, Preschool</topic><topic>Cyclin-dependent kinase inhibitor p21</topic><topic>Cyclin-Dependent Kinase Inhibitor p21 - genetics</topic><topic>Cyclin-Dependent Kinase Inhibitor p21 - metabolism</topic><topic>Cyclin-dependent kinases</topic><topic>Development and progression</topic><topic>Enzyme inhibitors</topic><topic>Female</topic><topic>Gene expression</topic><topic>Gene Expression Regulation, Neoplastic - drug effects</topic><topic>Gene silencing</topic><topic>Genetic aspects</topic><topic>GTP-binding protein</topic><topic>Health aspects</topic><topic>Humans</topic><topic>Immunohistochemistry</topic><topic>Kinases</topic><topic>Male</topic><topic>Middle Aged</topic><topic>Musculoskeletal system</topic><topic>Myc protein</topic><topic>Oncogenes</topic><topic>Polymerase chain reaction</topic><topic>Proteins</topic><topic>Proto-Oncogene Proteins c-myc - metabolism</topic><topic>Reverse transcription</topic><topic>Rhabdomyosarcoma</topic><topic>Rhabdomyosarcoma - genetics</topic><topic>Rhabdomyosarcoma - metabolism</topic><topic>Rhabdomyosarcoma - pathology</topic><topic>RNA, Messenger - genetics</topic><topic>RNA, Messenger - metabolism</topic><topic>Skeletal muscle</topic><topic>Thiazoles - pharmacology</topic><topic>Transcription, Genetic - drug effects</topic><topic>Tumorigenesis</topic><topic>Tumors</topic><topic>Western blotting</topic><topic>Young Adult</topic><toplevel>online_resources</toplevel><creatorcontrib>Zhang, Jinghang</creatorcontrib><creatorcontrib>Song, Na</creatorcontrib><creatorcontrib>Zang, Dan</creatorcontrib><creatorcontrib>Yu, Jian</creatorcontrib><creatorcontrib>Li, Jinsong</creatorcontrib><creatorcontrib>Di, Wenyu</creatorcontrib><creatorcontrib>Guo, Ruina</creatorcontrib><creatorcontrib>Zhao, Weixing</creatorcontrib><creatorcontrib>Wang, Haijun</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>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</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>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>British Nursing Database</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>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>Biological Science 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>MEDLINE - Academic</collection><jtitle>Molecular medicine reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhang, Jinghang</au><au>Song, Na</au><au>Zang, Dan</au><au>Yu, Jian</au><au>Li, Jinsong</au><au>Di, Wenyu</au><au>Guo, Ruina</au><au>Zhao, Weixing</au><au>Wang, Haijun</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>c-Myc promotes tumor proliferation and anti‑apoptosis by repressing p21 in rhabdomyosarcomas</atitle><jtitle>Molecular medicine reports</jtitle><addtitle>Mol Med Rep</addtitle><date>2017-10-01</date><risdate>2017</risdate><volume>16</volume><issue>4</issue><spage>4089</spage><epage>4094</epage><pages>4089-4094</pages><issn>1791-2997</issn><eissn>1791-3004</eissn><abstract>v-myc avian myelocytomatosis viral oncogene homolog (c-Myc) is an important member protein of the Myc family that is important in cell cycle progression, apoptosis and tumorigenesis. In the present study, the role of c‑Myc in rhabdomyosarcoma (RMS) was assessed. Firstly, expression of endogenous c‑Myc and cyclin dependent kinase inhibitor 1A (p21) was examined in normal skeletal muscle, RMS specimens and TE671 RMS cells by immunohistochemistry, reverse transcription‑quantitative polymerase chain reaction and western blotting. Furthermore, cell cycle progression and apoptosis were assessed in TE671 RMS cells following treatment with a c‑Myc inhibitor, 10058‑F4. The results demonstrated that c‑Myc was overexpressed in clinical RMS tissues and TE671 cells, with the highest expression observed in the most RMS samples. Expression of p21 protein and apoptosis function were increased following treatment with 10058‑F4, but no difference was observed in cell cycle progression. In conclusion, the present study indicated that c‑Myc promotes RMS development by inhibiting apoptosis through repression of p21 transcription. Further studies will be required to evaluate c‑Myc as a target for RMS clinical treatment.</abstract><cop>Greece</cop><pub>Spandidos Publications</pub><pmid>28765944</pmid><doi>10.3892/mmr.2017.7101</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Adolescent Aged Apoptosis Biotechnology c-Myc protein Cancer Carcinogenesis - genetics Carcinogenesis - pathology Care and treatment Cell cycle Cell Cycle - genetics Cell growth Cell Line, Tumor Cell Proliferation Child Child, Preschool Cyclin-dependent kinase inhibitor p21 Cyclin-Dependent Kinase Inhibitor p21 - genetics Cyclin-Dependent Kinase Inhibitor p21 - metabolism Cyclin-dependent kinases Development and progression Enzyme inhibitors Female Gene expression Gene Expression Regulation, Neoplastic - drug effects Gene silencing Genetic aspects GTP-binding protein Health aspects Humans Immunohistochemistry Kinases Male Middle Aged Musculoskeletal system Myc protein Oncogenes Polymerase chain reaction Proteins Proto-Oncogene Proteins c-myc - metabolism Reverse transcription Rhabdomyosarcoma Rhabdomyosarcoma - genetics Rhabdomyosarcoma - metabolism Rhabdomyosarcoma - pathology RNA, Messenger - genetics RNA, Messenger - metabolism Skeletal muscle Thiazoles - pharmacology Transcription, Genetic - drug effects Tumorigenesis Tumors Western blotting Young Adult |
| title | c-Myc promotes tumor proliferation and anti‑apoptosis by repressing p21 in rhabdomyosarcomas |
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