Survivin: A novel marker and potential therapeutic target for human angiosarcoma
Human angiosarcoma is a rare malignant vascular tumor associated with extremely poor clinical outcome and generally arising in skin of the head and neck region. However, little is known about the molecular pathogeneses and useful immunohistochemical markers of angiosarcoma. To investigate the mechan...
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| Veröffentlicht in: | Cancer science 2017-11, Vol.108 (11), p.2295-2305 |
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| creator | Tsuneki, Masayuki Kinjo, Takao Mori, Taisuke Yoshida, Akihiko Kuyama, Kayo Ohira, Aoi Miyagi, Takuya Takahashi, Kenzo Kawai, Akira Chuman, Hirokazu Yamazaki, Naoya Masuzawa, Mikio Arakawa, Hirofumi |
| description | Human angiosarcoma is a rare malignant vascular tumor associated with extremely poor clinical outcome and generally arising in skin of the head and neck region. However, little is known about the molecular pathogeneses and useful immunohistochemical markers of angiosarcoma. To investigate the mechanisms of angiosarcoma progression, we collected 85 cases of human angiosarcoma specimens with clinical records and analyzed ISO‐HAS‐B patient‐derived angiosarcoma cells. As control subjects, 54 cases of hemangioma and 34 of pyogenic granuloma were collected. Remarkably, consistent with our recent observations regarding the involvement of survivin expression following Hippo pathway inactivation in the neoplastic proliferation of murine hemangioendothelioma cells and human infantile hemangioma, nuclear survivin expression was observed in all cases of angiosarcoma but not in hemangiomas and pyogenic granulomas, and the Hippo pathway was inactivated in 90.3% of yes‐associated protein (YAP) ‐positive angiosarcoma cases. However, survivin expression modes and YAP localization (Hippo pathway activation modes) were not correlated with survival. In addition, we confirmed that survivin small interference RNA (siRNA) transfection and YM155, an anti‐survivin drug, elicited decreased nuclear survivin expression and cell proliferation in ISO‐HAS‐B cells which expressed survivin consistently. Conclusively, these findings support the importance of survivin as a good marker and critical regulator of cellular proliferation for human angiosarcoma and YM155 as a potential therapeutic agent.
Our findings support the importance of Survivin as a good marker and critical regulator of cellular proliferation for human angiosarcoma and YM155 as a potential therapeutic agent |
| doi_str_mv | 10.1111/cas.13379 |
| format | Article |
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Our findings support the importance of Survivin as a good marker and critical regulator of cellular proliferation for human angiosarcoma and YM155 as a potential therapeutic agent</description><identifier>ISSN: 1347-9032</identifier><identifier>EISSN: 1349-7006</identifier><identifier>DOI: 10.1111/cas.13379</identifier><identifier>PMID: 28845553</identifier><language>eng</language><publisher>England: John Wiley & Sons, Inc</publisher><subject>Adaptor Proteins, Signal Transducing - genetics ; Adult ; Aged ; Aged, 80 and over ; Angiosarcoma ; Apoptosis - drug effects ; Biomarkers, Tumor - genetics ; Cancer ; Cell adhesion & migration ; Cell growth ; Cell Line, Tumor ; Cell proliferation ; Cell Proliferation - drug effects ; Cell Proliferation - genetics ; Female ; Gene amplification ; Gene Expression Regulation, Neoplastic - drug effects ; Granuloma ; Head and neck ; Hemangioma ; Hemangiosarcoma - genetics ; Hemangiosarcoma - pathology ; Hippo pathway ; Humans ; Imidazoles ; Inhibitor of Apoptosis Proteins - antagonists & inhibitors ; Inhibitor of Apoptosis Proteins - genetics ; Kinases ; Liver ; Localization ; Lymphocytes B ; Male ; Medical prognosis ; Metastasis ; Middle Aged ; Naphthoquinones ; Original ; Pathogenesis ; Phosphoproteins - genetics ; proliferation ; Protein-Serine-Threonine Kinases - genetics ; RNA-mediated interference ; Signal Transduction - genetics ; siRNA ; Skin ; Survivin ; Therapeutic applications ; Transcription Factors ; Transfection ; Tumors ; Yes-associated protein ; YM155</subject><ispartof>Cancer science, 2017-11, Vol.108 (11), p.2295-2305</ispartof><rights>2017 The Authors. published by John Wiley & Sons Australia, Ltd on behalf of Japanese Cancer Association.</rights><rights>2017 The Authors. Cancer Science published by John Wiley & Sons Australia, Ltd on behalf of Japanese Cancer Association.</rights><rights>2017. This work is published under http://creativecommons.org/licenses/by-nc/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5779-4838bfaa93b8d6cefc5d32e7188aec8c27ec97094adda4f5a230a8924faa063a3</citedby><cites>FETCH-LOGICAL-c5779-4838bfaa93b8d6cefc5d32e7188aec8c27ec97094adda4f5a230a8924faa063a3</cites><orcidid>0000-0001-6077-0638 ; 0000-0003-3409-5485 ; 0000-0002-9638-0428</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5665764/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5665764/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,1411,11541,27901,27902,45550,45551,46027,46451,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28845553$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Tsuneki, Masayuki</creatorcontrib><creatorcontrib>Kinjo, Takao</creatorcontrib><creatorcontrib>Mori, Taisuke</creatorcontrib><creatorcontrib>Yoshida, Akihiko</creatorcontrib><creatorcontrib>Kuyama, Kayo</creatorcontrib><creatorcontrib>Ohira, Aoi</creatorcontrib><creatorcontrib>Miyagi, Takuya</creatorcontrib><creatorcontrib>Takahashi, Kenzo</creatorcontrib><creatorcontrib>Kawai, Akira</creatorcontrib><creatorcontrib>Chuman, Hirokazu</creatorcontrib><creatorcontrib>Yamazaki, Naoya</creatorcontrib><creatorcontrib>Masuzawa, Mikio</creatorcontrib><creatorcontrib>Arakawa, Hirofumi</creatorcontrib><title>Survivin: A novel marker and potential therapeutic target for human angiosarcoma</title><title>Cancer science</title><addtitle>Cancer Sci</addtitle><description>Human angiosarcoma is a rare malignant vascular tumor associated with extremely poor clinical outcome and generally arising in skin of the head and neck region. However, little is known about the molecular pathogeneses and useful immunohistochemical markers of angiosarcoma. To investigate the mechanisms of angiosarcoma progression, we collected 85 cases of human angiosarcoma specimens with clinical records and analyzed ISO‐HAS‐B patient‐derived angiosarcoma cells. As control subjects, 54 cases of hemangioma and 34 of pyogenic granuloma were collected. Remarkably, consistent with our recent observations regarding the involvement of survivin expression following Hippo pathway inactivation in the neoplastic proliferation of murine hemangioendothelioma cells and human infantile hemangioma, nuclear survivin expression was observed in all cases of angiosarcoma but not in hemangiomas and pyogenic granulomas, and the Hippo pathway was inactivated in 90.3% of yes‐associated protein (YAP) ‐positive angiosarcoma cases. However, survivin expression modes and YAP localization (Hippo pathway activation modes) were not correlated with survival. In addition, we confirmed that survivin small interference RNA (siRNA) transfection and YM155, an anti‐survivin drug, elicited decreased nuclear survivin expression and cell proliferation in ISO‐HAS‐B cells which expressed survivin consistently. Conclusively, these findings support the importance of survivin as a good marker and critical regulator of cellular proliferation for human angiosarcoma and YM155 as a potential therapeutic agent.
Our findings support the importance of Survivin as a good marker and critical regulator of cellular proliferation for human angiosarcoma and YM155 as a potential therapeutic agent</description><subject>Adaptor Proteins, Signal Transducing - genetics</subject><subject>Adult</subject><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>Angiosarcoma</subject><subject>Apoptosis - drug effects</subject><subject>Biomarkers, Tumor - genetics</subject><subject>Cancer</subject><subject>Cell adhesion & migration</subject><subject>Cell growth</subject><subject>Cell Line, Tumor</subject><subject>Cell proliferation</subject><subject>Cell Proliferation - drug effects</subject><subject>Cell Proliferation - genetics</subject><subject>Female</subject><subject>Gene amplification</subject><subject>Gene Expression Regulation, Neoplastic - drug effects</subject><subject>Granuloma</subject><subject>Head and neck</subject><subject>Hemangioma</subject><subject>Hemangiosarcoma - genetics</subject><subject>Hemangiosarcoma - pathology</subject><subject>Hippo pathway</subject><subject>Humans</subject><subject>Imidazoles</subject><subject>Inhibitor of Apoptosis Proteins - antagonists & inhibitors</subject><subject>Inhibitor of Apoptosis Proteins - genetics</subject><subject>Kinases</subject><subject>Liver</subject><subject>Localization</subject><subject>Lymphocytes B</subject><subject>Male</subject><subject>Medical prognosis</subject><subject>Metastasis</subject><subject>Middle Aged</subject><subject>Naphthoquinones</subject><subject>Original</subject><subject>Pathogenesis</subject><subject>Phosphoproteins - genetics</subject><subject>proliferation</subject><subject>Protein-Serine-Threonine Kinases - genetics</subject><subject>RNA-mediated interference</subject><subject>Signal Transduction - genetics</subject><subject>siRNA</subject><subject>Skin</subject><subject>Survivin</subject><subject>Therapeutic applications</subject><subject>Transcription Factors</subject><subject>Transfection</subject><subject>Tumors</subject><subject>Yes-associated protein</subject><subject>YM155</subject><issn>1347-9032</issn><issn>1349-7006</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>24P</sourceid><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNp1kMtKAzEUhoMo3he-gARcuRjN5DJJXAileANBoboOp5lMG51Oamam0rc3tiq6MJsTyHe-_PwIHeXkLE_n3EJ7ljMm9QbazRnXmSSk2FzdZaYJoztor21fCGEF13wb7VCluBCC7aLHUR8XfuGbCzzATVi4Gs8gvrqIoSnxPHSu6TzUuJu6CHPXd97iDuLEdbgKEU_7GTQJnfjQQrRhBgdoq4K6dYdfcx89X189DW-z-4ebu-HgPrNCSp1xxdS4AtBsrMrCusqKklEnc6XAWWWpdFZLojmUJfBKAGUElKY87ZCCAdtHl2vvvB_PXGlTzgi1mUef8i9NAG_-vjR-aiZhYURRCFnwJDj5EsTw1ru2My-hj03KbChVWlIqGEnU6ZqyMbRtdNXPDzkxn-WbVL5ZlZ_Y49-RfsjvthNwvgbefe2W_5vMcDBaKz8A7giQcA</recordid><startdate>201711</startdate><enddate>201711</enddate><creator>Tsuneki, Masayuki</creator><creator>Kinjo, Takao</creator><creator>Mori, Taisuke</creator><creator>Yoshida, Akihiko</creator><creator>Kuyama, Kayo</creator><creator>Ohira, Aoi</creator><creator>Miyagi, Takuya</creator><creator>Takahashi, Kenzo</creator><creator>Kawai, Akira</creator><creator>Chuman, Hirokazu</creator><creator>Yamazaki, Naoya</creator><creator>Masuzawa, Mikio</creator><creator>Arakawa, Hirofumi</creator><general>John Wiley & Sons, Inc</general><general>John Wiley and Sons Inc</general><scope>24P</scope><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>8FE</scope><scope>8FH</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>GNUQQ</scope><scope>HCIFZ</scope><scope>LK8</scope><scope>M7P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0001-6077-0638</orcidid><orcidid>https://orcid.org/0000-0003-3409-5485</orcidid><orcidid>https://orcid.org/0000-0002-9638-0428</orcidid></search><sort><creationdate>201711</creationdate><title>Survivin: A novel marker and potential therapeutic target for human angiosarcoma</title><author>Tsuneki, Masayuki ; Kinjo, Takao ; Mori, Taisuke ; Yoshida, Akihiko ; Kuyama, Kayo ; Ohira, Aoi ; Miyagi, Takuya ; Takahashi, Kenzo ; Kawai, Akira ; Chuman, Hirokazu ; Yamazaki, Naoya ; Masuzawa, Mikio ; Arakawa, Hirofumi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5779-4838bfaa93b8d6cefc5d32e7188aec8c27ec97094adda4f5a230a8924faa063a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Adaptor Proteins, Signal Transducing - genetics</topic><topic>Adult</topic><topic>Aged</topic><topic>Aged, 80 and over</topic><topic>Angiosarcoma</topic><topic>Apoptosis - drug effects</topic><topic>Biomarkers, Tumor - genetics</topic><topic>Cancer</topic><topic>Cell adhesion & migration</topic><topic>Cell growth</topic><topic>Cell Line, Tumor</topic><topic>Cell proliferation</topic><topic>Cell Proliferation - drug effects</topic><topic>Cell Proliferation - genetics</topic><topic>Female</topic><topic>Gene amplification</topic><topic>Gene Expression Regulation, Neoplastic - drug effects</topic><topic>Granuloma</topic><topic>Head and neck</topic><topic>Hemangioma</topic><topic>Hemangiosarcoma - genetics</topic><topic>Hemangiosarcoma - pathology</topic><topic>Hippo pathway</topic><topic>Humans</topic><topic>Imidazoles</topic><topic>Inhibitor of Apoptosis Proteins - antagonists & inhibitors</topic><topic>Inhibitor of Apoptosis Proteins - genetics</topic><topic>Kinases</topic><topic>Liver</topic><topic>Localization</topic><topic>Lymphocytes B</topic><topic>Male</topic><topic>Medical prognosis</topic><topic>Metastasis</topic><topic>Middle Aged</topic><topic>Naphthoquinones</topic><topic>Original</topic><topic>Pathogenesis</topic><topic>Phosphoproteins - genetics</topic><topic>proliferation</topic><topic>Protein-Serine-Threonine Kinases - genetics</topic><topic>RNA-mediated interference</topic><topic>Signal Transduction - genetics</topic><topic>siRNA</topic><topic>Skin</topic><topic>Survivin</topic><topic>Therapeutic applications</topic><topic>Transcription Factors</topic><topic>Transfection</topic><topic>Tumors</topic><topic>Yes-associated protein</topic><topic>YM155</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Tsuneki, Masayuki</creatorcontrib><creatorcontrib>Kinjo, Takao</creatorcontrib><creatorcontrib>Mori, Taisuke</creatorcontrib><creatorcontrib>Yoshida, Akihiko</creatorcontrib><creatorcontrib>Kuyama, Kayo</creatorcontrib><creatorcontrib>Ohira, Aoi</creatorcontrib><creatorcontrib>Miyagi, Takuya</creatorcontrib><creatorcontrib>Takahashi, Kenzo</creatorcontrib><creatorcontrib>Kawai, Akira</creatorcontrib><creatorcontrib>Chuman, Hirokazu</creatorcontrib><creatorcontrib>Yamazaki, Naoya</creatorcontrib><creatorcontrib>Masuzawa, Mikio</creatorcontrib><creatorcontrib>Arakawa, Hirofumi</creatorcontrib><collection>Wiley Online Library Open Access</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</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>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Biological Science Collection</collection><collection>Biological Science Database</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>PubMed Central (Full Participant titles)</collection><jtitle>Cancer science</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Tsuneki, Masayuki</au><au>Kinjo, Takao</au><au>Mori, Taisuke</au><au>Yoshida, Akihiko</au><au>Kuyama, Kayo</au><au>Ohira, Aoi</au><au>Miyagi, Takuya</au><au>Takahashi, Kenzo</au><au>Kawai, Akira</au><au>Chuman, Hirokazu</au><au>Yamazaki, Naoya</au><au>Masuzawa, Mikio</au><au>Arakawa, Hirofumi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Survivin: A novel marker and potential therapeutic target for human angiosarcoma</atitle><jtitle>Cancer science</jtitle><addtitle>Cancer Sci</addtitle><date>2017-11</date><risdate>2017</risdate><volume>108</volume><issue>11</issue><spage>2295</spage><epage>2305</epage><pages>2295-2305</pages><issn>1347-9032</issn><eissn>1349-7006</eissn><abstract>Human angiosarcoma is a rare malignant vascular tumor associated with extremely poor clinical outcome and generally arising in skin of the head and neck region. However, little is known about the molecular pathogeneses and useful immunohistochemical markers of angiosarcoma. To investigate the mechanisms of angiosarcoma progression, we collected 85 cases of human angiosarcoma specimens with clinical records and analyzed ISO‐HAS‐B patient‐derived angiosarcoma cells. As control subjects, 54 cases of hemangioma and 34 of pyogenic granuloma were collected. Remarkably, consistent with our recent observations regarding the involvement of survivin expression following Hippo pathway inactivation in the neoplastic proliferation of murine hemangioendothelioma cells and human infantile hemangioma, nuclear survivin expression was observed in all cases of angiosarcoma but not in hemangiomas and pyogenic granulomas, and the Hippo pathway was inactivated in 90.3% of yes‐associated protein (YAP) ‐positive angiosarcoma cases. However, survivin expression modes and YAP localization (Hippo pathway activation modes) were not correlated with survival. In addition, we confirmed that survivin small interference RNA (siRNA) transfection and YM155, an anti‐survivin drug, elicited decreased nuclear survivin expression and cell proliferation in ISO‐HAS‐B cells which expressed survivin consistently. Conclusively, these findings support the importance of survivin as a good marker and critical regulator of cellular proliferation for human angiosarcoma and YM155 as a potential therapeutic agent.
Our findings support the importance of Survivin as a good marker and critical regulator of cellular proliferation for human angiosarcoma and YM155 as a potential therapeutic agent</abstract><cop>England</cop><pub>John Wiley & Sons, Inc</pub><pmid>28845553</pmid><doi>10.1111/cas.13379</doi><tpages>11</tpages><orcidid>https://orcid.org/0000-0001-6077-0638</orcidid><orcidid>https://orcid.org/0000-0003-3409-5485</orcidid><orcidid>https://orcid.org/0000-0002-9638-0428</orcidid><oa>free_for_read</oa></addata></record> |
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| ispartof | Cancer science, 2017-11, Vol.108 (11), p.2295-2305 |
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| language | eng |
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| source | MEDLINE; Wiley Online Library Open Access; DOAJ Directory of Open Access Journals; Wiley Online Library Journals Frontfile Complete; PubMed Central |
| subjects | Adaptor Proteins, Signal Transducing - genetics Adult Aged Aged, 80 and over Angiosarcoma Apoptosis - drug effects Biomarkers, Tumor - genetics Cancer Cell adhesion & migration Cell growth Cell Line, Tumor Cell proliferation Cell Proliferation - drug effects Cell Proliferation - genetics Female Gene amplification Gene Expression Regulation, Neoplastic - drug effects Granuloma Head and neck Hemangioma Hemangiosarcoma - genetics Hemangiosarcoma - pathology Hippo pathway Humans Imidazoles Inhibitor of Apoptosis Proteins - antagonists & inhibitors Inhibitor of Apoptosis Proteins - genetics Kinases Liver Localization Lymphocytes B Male Medical prognosis Metastasis Middle Aged Naphthoquinones Original Pathogenesis Phosphoproteins - genetics proliferation Protein-Serine-Threonine Kinases - genetics RNA-mediated interference Signal Transduction - genetics siRNA Skin Survivin Therapeutic applications Transcription Factors Transfection Tumors Yes-associated protein YM155 |
| title | Survivin: A novel marker and potential therapeutic target for human angiosarcoma |
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