CTC1 increases the radioresistance of human melanoma cells by inhibiting telomere shortening and apoptosis
Melanoma has traditionally been viewed as a radioresistant cancer. However, recent studies suggest that under certain clinical circumstances, radiotherapy may play a significant role in the treatment of melanoma. Previous studies have demonstrated that telomere length is a hallmark of radiosensitivi...
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| Veröffentlicht in: | International journal of molecular medicine 2014-06, Vol.33 (6), p.1484-1490 |
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| container_title | International journal of molecular medicine |
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| creator | LUO, Y.M XIA, N.X YANG, L LI, Z YANG, H YU, H.J LIU, Y LEI, H ZHOU, F.X XIE, C.H ZHOU, Y.F |
| description | Melanoma has traditionally been viewed as a radioresistant cancer. However, recent studies suggest that under certain clinical circumstances, radiotherapy may play a significant role in the treatment of melanoma. Previous studies have demonstrated that telomere length is a hallmark of radiosensitivity. The newly discovered mammalian CTC1-STN1-TEN1 (CST) complex has been demonstrated to be an important telomere maintenance factor. In this study, by establishing a radiosensitive/radioresistant human melanoma cell model, MDA-MB-435/MDA-MB-435R, we aimed to investigate the association of CTC1 expression with radiosensitivity in human melanoma cell lines, and to elucidate the possible underlying mechanisms. We found that CTC1 mRNA and protein levels were markedly increased in the MDA-MB-435R cells compared with the MDA-MB-435 cells. Moreover, the downregulation of CTC1 enhanced radiosensitivity, induced DNA damage and promoted telomere shortening and apoptosis in both cell lines. Taken together, our findings suggest that CTC1 increases the radioresistance of human melanoma cells by inhibiting telomere shortening and apoptosis. Thus, CTC1 may be an attractive target gene for the treatment of human melanoma. |
| doi_str_mv | 10.3892/ijmm.2014.1721 |
| format | Article |
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However, recent studies suggest that under certain clinical circumstances, radiotherapy may play a significant role in the treatment of melanoma. Previous studies have demonstrated that telomere length is a hallmark of radiosensitivity. The newly discovered mammalian CTC1-STN1-TEN1 (CST) complex has been demonstrated to be an important telomere maintenance factor. In this study, by establishing a radiosensitive/radioresistant human melanoma cell model, MDA-MB-435/MDA-MB-435R, we aimed to investigate the association of CTC1 expression with radiosensitivity in human melanoma cell lines, and to elucidate the possible underlying mechanisms. We found that CTC1 mRNA and protein levels were markedly increased in the MDA-MB-435R cells compared with the MDA-MB-435 cells. Moreover, the downregulation of CTC1 enhanced radiosensitivity, induced DNA damage and promoted telomere shortening and apoptosis in both cell lines. Taken together, our findings suggest that CTC1 increases the radioresistance of human melanoma cells by inhibiting telomere shortening and apoptosis. Thus, CTC1 may be an attractive target gene for the treatment of human melanoma.</description><identifier>ISSN: 1107-3756</identifier><identifier>EISSN: 1791-244X</identifier><identifier>DOI: 10.3892/ijmm.2014.1721</identifier><identifier>PMID: 24718655</identifier><language>eng</language><publisher>Greece: D.A. Spandidos</publisher><subject>Analysis ; Apoptosis ; Apoptosis - genetics ; Apoptosis - physiology ; Biotechnology ; Care and treatment ; Cell Line, Tumor ; conserved telomere maintenance component 1 ; Defects ; Deoxyribonucleic acid ; DNA ; DNA Breaks, Double-Stranded ; Genetic aspects ; Humans ; Melanoma ; Melanoma - genetics ; Melanoma - metabolism ; Mutation ; Proteins ; radioresistance ; Skin cancer ; Studies ; Telomerase ; Telomere - genetics ; Telomere - metabolism ; Telomere Shortening - genetics ; Telomere Shortening - physiology ; telomere-binding protein ; Telomere-Binding Proteins - genetics ; Telomere-Binding Proteins - metabolism ; Telomeres</subject><ispartof>International journal of molecular medicine, 2014-06, Vol.33 (6), p.1484-1490</ispartof><rights>Copyright © 2014, Spandidos Publications</rights><rights>COPYRIGHT 2014 Spandidos Publications</rights><rights>Copyright Spandidos Publications UK Ltd. 2014</rights><rights>Copyright © 2014, Spandidos Publications 2014</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c518t-3bdfb579768c6c4a70adee05fa752af11defa8955f01f5dfa760233d4b4cce993</citedby><cites>FETCH-LOGICAL-c518t-3bdfb579768c6c4a70adee05fa752af11defa8955f01f5dfa760233d4b4cce993</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,776,780,881,5556,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24718655$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>LUO, Y.M</creatorcontrib><creatorcontrib>XIA, N.X</creatorcontrib><creatorcontrib>YANG, L</creatorcontrib><creatorcontrib>LI, Z</creatorcontrib><creatorcontrib>YANG, H</creatorcontrib><creatorcontrib>YU, H.J</creatorcontrib><creatorcontrib>LIU, Y</creatorcontrib><creatorcontrib>LEI, H</creatorcontrib><creatorcontrib>ZHOU, F.X</creatorcontrib><creatorcontrib>XIE, C.H</creatorcontrib><creatorcontrib>ZHOU, Y.F</creatorcontrib><title>CTC1 increases the radioresistance of human melanoma cells by inhibiting telomere shortening and apoptosis</title><title>International journal of molecular medicine</title><addtitle>Int J Mol Med</addtitle><description>Melanoma has traditionally been viewed as a radioresistant cancer. However, recent studies suggest that under certain clinical circumstances, radiotherapy may play a significant role in the treatment of melanoma. Previous studies have demonstrated that telomere length is a hallmark of radiosensitivity. The newly discovered mammalian CTC1-STN1-TEN1 (CST) complex has been demonstrated to be an important telomere maintenance factor. In this study, by establishing a radiosensitive/radioresistant human melanoma cell model, MDA-MB-435/MDA-MB-435R, we aimed to investigate the association of CTC1 expression with radiosensitivity in human melanoma cell lines, and to elucidate the possible underlying mechanisms. We found that CTC1 mRNA and protein levels were markedly increased in the MDA-MB-435R cells compared with the MDA-MB-435 cells. Moreover, the downregulation of CTC1 enhanced radiosensitivity, induced DNA damage and promoted telomere shortening and apoptosis in both cell lines. Taken together, our findings suggest that CTC1 increases the radioresistance of human melanoma cells by inhibiting telomere shortening and apoptosis. Thus, CTC1 may be an attractive target gene for the treatment of human melanoma.</description><subject>Analysis</subject><subject>Apoptosis</subject><subject>Apoptosis - genetics</subject><subject>Apoptosis - physiology</subject><subject>Biotechnology</subject><subject>Care and treatment</subject><subject>Cell Line, Tumor</subject><subject>conserved telomere maintenance component 1</subject><subject>Defects</subject><subject>Deoxyribonucleic acid</subject><subject>DNA</subject><subject>DNA Breaks, Double-Stranded</subject><subject>Genetic aspects</subject><subject>Humans</subject><subject>Melanoma</subject><subject>Melanoma - genetics</subject><subject>Melanoma - metabolism</subject><subject>Mutation</subject><subject>Proteins</subject><subject>radioresistance</subject><subject>Skin cancer</subject><subject>Studies</subject><subject>Telomerase</subject><subject>Telomere - genetics</subject><subject>Telomere - metabolism</subject><subject>Telomere Shortening - genetics</subject><subject>Telomere Shortening - physiology</subject><subject>telomere-binding protein</subject><subject>Telomere-Binding Proteins - genetics</subject><subject>Telomere-Binding Proteins - metabolism</subject><subject>Telomeres</subject><issn>1107-3756</issn><issn>1791-244X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNptkc2L1TAUxYsozji6dSkBN276TJqkaTbC8PALBtyM4C6kyc1rHk1Skz5h_ntTZnwqDFkknJzz415O07wmeEcH2b33xxB2HSZsR0RHnjSXREjSdoz9eFrfBIuWCt5fNC9KOWLccSaH581FxwQZes4vm-P-dk-QjyaDLlDQOgHK2vqUofiy6mgAJYemU9ARBZh1TEEjA_Nc0HhXg5Mf_erjAa0wpwAZUJlSXiFumo4W6SUta6qwl80zp-cCrx7uq-b7p4-3-y_tzbfPX_fXN63hZFhbOlo3ciFFP5jeMC2wtgCYOy14px0hFpweJOcOE8dtlXvcUWrZyIwBKelV8-Geu5zGANZAXLOe1ZJ90PlOJe3V_z_RT-qQfimGOWeUVMDbB0BOP09QVnVMpxzrzIpI2lHGsKR_XQc9g_LRpQozwRejrhmhROCh31i7R1z1WAjepAjOV_2xgMmplAzuPDjBaqtcbZWrrXK1VV4Db_5d92z_03E1vLs3lKX24W0qZ8-Gailtcd8SNjD6Gxuvtwo</recordid><startdate>20140601</startdate><enddate>20140601</enddate><creator>LUO, Y.M</creator><creator>XIA, N.X</creator><creator>YANG, L</creator><creator>LI, Z</creator><creator>YANG, H</creator><creator>YU, H.J</creator><creator>LIU, Y</creator><creator>LEI, H</creator><creator>ZHOU, F.X</creator><creator>XIE, C.H</creator><creator>ZHOU, Y.F</creator><general>D.A. 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genetics</topic><topic>Apoptosis - physiology</topic><topic>Biotechnology</topic><topic>Care and treatment</topic><topic>Cell Line, Tumor</topic><topic>conserved telomere maintenance component 1</topic><topic>Defects</topic><topic>Deoxyribonucleic acid</topic><topic>DNA</topic><topic>DNA Breaks, Double-Stranded</topic><topic>Genetic aspects</topic><topic>Humans</topic><topic>Melanoma</topic><topic>Melanoma - genetics</topic><topic>Melanoma - metabolism</topic><topic>Mutation</topic><topic>Proteins</topic><topic>radioresistance</topic><topic>Skin cancer</topic><topic>Studies</topic><topic>Telomerase</topic><topic>Telomere - genetics</topic><topic>Telomere - metabolism</topic><topic>Telomere Shortening - genetics</topic><topic>Telomere Shortening - physiology</topic><topic>telomere-binding protein</topic><topic>Telomere-Binding Proteins - genetics</topic><topic>Telomere-Binding Proteins - metabolism</topic><topic>Telomeres</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>LUO, Y.M</creatorcontrib><creatorcontrib>XIA, N.X</creatorcontrib><creatorcontrib>YANG, L</creatorcontrib><creatorcontrib>LI, Z</creatorcontrib><creatorcontrib>YANG, H</creatorcontrib><creatorcontrib>YU, H.J</creatorcontrib><creatorcontrib>LIU, Y</creatorcontrib><creatorcontrib>LEI, H</creatorcontrib><creatorcontrib>ZHOU, F.X</creatorcontrib><creatorcontrib>XIE, C.H</creatorcontrib><creatorcontrib>ZHOU, Y.F</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>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>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</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>ProQuest Central China</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>International journal of molecular medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>LUO, Y.M</au><au>XIA, N.X</au><au>YANG, L</au><au>LI, Z</au><au>YANG, H</au><au>YU, H.J</au><au>LIU, Y</au><au>LEI, H</au><au>ZHOU, F.X</au><au>XIE, C.H</au><au>ZHOU, Y.F</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>CTC1 increases the radioresistance of human melanoma cells by inhibiting telomere shortening and apoptosis</atitle><jtitle>International journal of molecular medicine</jtitle><addtitle>Int J Mol Med</addtitle><date>2014-06-01</date><risdate>2014</risdate><volume>33</volume><issue>6</issue><spage>1484</spage><epage>1490</epage><pages>1484-1490</pages><issn>1107-3756</issn><eissn>1791-244X</eissn><abstract>Melanoma has traditionally been viewed as a radioresistant cancer. However, recent studies suggest that under certain clinical circumstances, radiotherapy may play a significant role in the treatment of melanoma. Previous studies have demonstrated that telomere length is a hallmark of radiosensitivity. The newly discovered mammalian CTC1-STN1-TEN1 (CST) complex has been demonstrated to be an important telomere maintenance factor. In this study, by establishing a radiosensitive/radioresistant human melanoma cell model, MDA-MB-435/MDA-MB-435R, we aimed to investigate the association of CTC1 expression with radiosensitivity in human melanoma cell lines, and to elucidate the possible underlying mechanisms. We found that CTC1 mRNA and protein levels were markedly increased in the MDA-MB-435R cells compared with the MDA-MB-435 cells. Moreover, the downregulation of CTC1 enhanced radiosensitivity, induced DNA damage and promoted telomere shortening and apoptosis in both cell lines. Taken together, our findings suggest that CTC1 increases the radioresistance of human melanoma cells by inhibiting telomere shortening and apoptosis. Thus, CTC1 may be an attractive target gene for the treatment of human melanoma.</abstract><cop>Greece</cop><pub>D.A. Spandidos</pub><pmid>24718655</pmid><doi>10.3892/ijmm.2014.1721</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| source | Spandidos Publications Journals; MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Alma/SFX Local Collection |
| subjects | Analysis Apoptosis Apoptosis - genetics Apoptosis - physiology Biotechnology Care and treatment Cell Line, Tumor conserved telomere maintenance component 1 Defects Deoxyribonucleic acid DNA DNA Breaks, Double-Stranded Genetic aspects Humans Melanoma Melanoma - genetics Melanoma - metabolism Mutation Proteins radioresistance Skin cancer Studies Telomerase Telomere - genetics Telomere - metabolism Telomere Shortening - genetics Telomere Shortening - physiology telomere-binding protein Telomere-Binding Proteins - genetics Telomere-Binding Proteins - metabolism Telomeres |
| title | CTC1 increases the radioresistance of human melanoma cells by inhibiting telomere shortening and apoptosis |
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