Oncogenic histone methyltransferase EZH2: A novel prognostic marker with therapeutic potential in endometrial cancer
The histone methyltransferase EZH2, a key epigenetic modifier, is known to be associated with human tumorigenesis. However, the physiological importance of EZH2 and its clinical relevance in endometrial cancer remain unclear. Hence, in the present study, we investigated the expression and function o...
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| Veröffentlicht in: | Oncotarget 2017-06, Vol.8 (25), p.40402-40411 |
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| creator | Oki, Shinya Sone, Kenbun Oda, Katsutoshi Hamamoto, Ryuji Ikemura, Masako Maeda, Daichi Takeuchi, Makoto Tanikawa, Michihiro Mori-Uchino, Mayuyo Nagasaka, Kazunori Miyasaka, Aki Kashiyama, Tomoko Ikeda, Yuji Arimoto, Takahide Kuramoto, Hiroyuki Wada-Hiraike, Osamu Kawana, Kei Fukayama, Masashi Osuga, Yutaka Fujii, Tomoyuki |
| description | The histone methyltransferase EZH2, a key epigenetic modifier, is known to be associated with human tumorigenesis. However, the physiological importance of EZH2 and its clinical relevance in endometrial cancer remain unclear. Hence, in the present study, we investigated the expression and function of EZH2 in endometrial cancer. In a quantitative real-time PCR analysis of 11 endometrial cancer cell lines and 52 clinical endometrial cancer specimens, EZH2 was significantly overexpressed in cancer cells and tissues compared to that in corresponding normal control cells and tissues. Kaplan-Meier survival analysis using data of the TCGA RNA-seq database and tissue microarrays (TMAs) indicated that EZH2 overexpression is associated with endometrial cancer prognosis. In addition, knockdown of EZH2 using specific siRNAs resulted in growth suppression and apoptosis induction of endometrial cancer cells, accompanied by attenuation of H3K27 trimethylation. Consistent with these results, treatment with GSK126, a specific EZH2 inhibitor, suppressed endometrial cancer cell growth and decreased the number of cancer cell colonies. Furthermore, GSK126 showed additive effects with doxorubicin or cisplatin, which are conventional drugs for treatment of endometrial cancer. Further studies should explore the therapeutic potential of inhibiting EZH2 in patients with endometrial cancer. |
| doi_str_mv | 10.18632/oncotarget.16316 |
| format | Article |
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However, the physiological importance of EZH2 and its clinical relevance in endometrial cancer remain unclear. Hence, in the present study, we investigated the expression and function of EZH2 in endometrial cancer. In a quantitative real-time PCR analysis of 11 endometrial cancer cell lines and 52 clinical endometrial cancer specimens, EZH2 was significantly overexpressed in cancer cells and tissues compared to that in corresponding normal control cells and tissues. Kaplan-Meier survival analysis using data of the TCGA RNA-seq database and tissue microarrays (TMAs) indicated that EZH2 overexpression is associated with endometrial cancer prognosis. In addition, knockdown of EZH2 using specific siRNAs resulted in growth suppression and apoptosis induction of endometrial cancer cells, accompanied by attenuation of H3K27 trimethylation. Consistent with these results, treatment with GSK126, a specific EZH2 inhibitor, suppressed endometrial cancer cell growth and decreased the number of cancer cell colonies. Furthermore, GSK126 showed additive effects with doxorubicin or cisplatin, which are conventional drugs for treatment of endometrial cancer. Further studies should explore the therapeutic potential of inhibiting EZH2 in patients with endometrial cancer.</description><identifier>ISSN: 1949-2553</identifier><identifier>EISSN: 1949-2553</identifier><identifier>DOI: 10.18632/oncotarget.16316</identifier><identifier>PMID: 28418882</identifier><language>eng</language><publisher>United States: Impact Journals LLC</publisher><subject>Antineoplastic Agents - pharmacology ; Antineoplastic Combined Chemotherapy Protocols - pharmacology ; Apoptosis - drug effects ; Apoptosis - genetics ; Biomarkers, Tumor - genetics ; Carcinogenesis - drug effects ; Carcinogenesis - genetics ; Cell Line, Tumor ; Cell Proliferation - drug effects ; Cell Proliferation - genetics ; Cisplatin - pharmacology ; Doxorubicin - pharmacology ; Endometrial Neoplasms - drug therapy ; Endometrial Neoplasms - genetics ; Endometrial Neoplasms - mortality ; Enhancer of Zeste Homolog 2 Protein - antagonists & inhibitors ; Enhancer of Zeste Homolog 2 Protein - genetics ; Enhancer of Zeste Homolog 2 Protein - metabolism ; Female ; Genetic Markers - genetics ; Histones - metabolism ; Humans ; Indoles - pharmacology ; Prognosis ; Pyridones - pharmacology ; Research Paper ; RNA Interference ; RNA, Small Interfering - genetics</subject><ispartof>Oncotarget, 2017-06, Vol.8 (25), p.40402-40411</ispartof><rights>Copyright: © 2017 Oki et al. 2017</rights><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c400t-1d6a82e5027c2368e00a66c596ad9bb01b4d2fe83d285f68fe62b2edb8bc799c3</citedby><cites>FETCH-LOGICAL-c400t-1d6a82e5027c2368e00a66c596ad9bb01b4d2fe83d285f68fe62b2edb8bc799c3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5522273/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5522273/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28418882$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Oki, Shinya</creatorcontrib><creatorcontrib>Sone, Kenbun</creatorcontrib><creatorcontrib>Oda, Katsutoshi</creatorcontrib><creatorcontrib>Hamamoto, Ryuji</creatorcontrib><creatorcontrib>Ikemura, Masako</creatorcontrib><creatorcontrib>Maeda, Daichi</creatorcontrib><creatorcontrib>Takeuchi, Makoto</creatorcontrib><creatorcontrib>Tanikawa, Michihiro</creatorcontrib><creatorcontrib>Mori-Uchino, Mayuyo</creatorcontrib><creatorcontrib>Nagasaka, Kazunori</creatorcontrib><creatorcontrib>Miyasaka, Aki</creatorcontrib><creatorcontrib>Kashiyama, Tomoko</creatorcontrib><creatorcontrib>Ikeda, Yuji</creatorcontrib><creatorcontrib>Arimoto, Takahide</creatorcontrib><creatorcontrib>Kuramoto, Hiroyuki</creatorcontrib><creatorcontrib>Wada-Hiraike, Osamu</creatorcontrib><creatorcontrib>Kawana, Kei</creatorcontrib><creatorcontrib>Fukayama, Masashi</creatorcontrib><creatorcontrib>Osuga, Yutaka</creatorcontrib><creatorcontrib>Fujii, Tomoyuki</creatorcontrib><title>Oncogenic histone methyltransferase EZH2: A novel prognostic marker with therapeutic potential in endometrial cancer</title><title>Oncotarget</title><addtitle>Oncotarget</addtitle><description>The histone methyltransferase EZH2, a key epigenetic modifier, is known to be associated with human tumorigenesis. However, the physiological importance of EZH2 and its clinical relevance in endometrial cancer remain unclear. Hence, in the present study, we investigated the expression and function of EZH2 in endometrial cancer. In a quantitative real-time PCR analysis of 11 endometrial cancer cell lines and 52 clinical endometrial cancer specimens, EZH2 was significantly overexpressed in cancer cells and tissues compared to that in corresponding normal control cells and tissues. Kaplan-Meier survival analysis using data of the TCGA RNA-seq database and tissue microarrays (TMAs) indicated that EZH2 overexpression is associated with endometrial cancer prognosis. In addition, knockdown of EZH2 using specific siRNAs resulted in growth suppression and apoptosis induction of endometrial cancer cells, accompanied by attenuation of H3K27 trimethylation. Consistent with these results, treatment with GSK126, a specific EZH2 inhibitor, suppressed endometrial cancer cell growth and decreased the number of cancer cell colonies. Furthermore, GSK126 showed additive effects with doxorubicin or cisplatin, which are conventional drugs for treatment of endometrial cancer. Further studies should explore the therapeutic potential of inhibiting EZH2 in patients with endometrial cancer.</description><subject>Antineoplastic Agents - pharmacology</subject><subject>Antineoplastic Combined Chemotherapy Protocols - pharmacology</subject><subject>Apoptosis - drug effects</subject><subject>Apoptosis - genetics</subject><subject>Biomarkers, Tumor - genetics</subject><subject>Carcinogenesis - drug effects</subject><subject>Carcinogenesis - genetics</subject><subject>Cell Line, Tumor</subject><subject>Cell Proliferation - drug effects</subject><subject>Cell Proliferation - genetics</subject><subject>Cisplatin - pharmacology</subject><subject>Doxorubicin - pharmacology</subject><subject>Endometrial Neoplasms - drug therapy</subject><subject>Endometrial Neoplasms - genetics</subject><subject>Endometrial Neoplasms - mortality</subject><subject>Enhancer of Zeste Homolog 2 Protein - antagonists & inhibitors</subject><subject>Enhancer of Zeste Homolog 2 Protein - genetics</subject><subject>Enhancer of Zeste Homolog 2 Protein - metabolism</subject><subject>Female</subject><subject>Genetic Markers - genetics</subject><subject>Histones - metabolism</subject><subject>Humans</subject><subject>Indoles - pharmacology</subject><subject>Prognosis</subject><subject>Pyridones - pharmacology</subject><subject>Research Paper</subject><subject>RNA Interference</subject><subject>RNA, Small Interfering - genetics</subject><issn>1949-2553</issn><issn>1949-2553</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpVkclOxSAYhYnRqFEfwI1h6eYqQ0vBhYkxTomJG924IZT-vUV7oQJX49uLs7JhOufjhIPQLiUHVArODoO3IZs4h3xABadiBW1SVakZq2u--me9gXZSeiBl1FUjmVpHG0xWVErJNlG-KZQ5eGfx4FIOHvAC8vA65mh86iGaBPjs_pId4RPswzOMeIph7kPKxbIw8REifnF5wHko4gmW7-dTyOCzMyN2HoPvQmHG96013kLcRmu9GRPsfM1b6O787Pb0cnZ9c3F1enI9sxUheUY7YSSDmrDGMi4kEGKEsLUSplNtS2hbdawHyTsm617IHgRrGXStbG2jlOVb6PiTOy3bBXS2ZIpm1FN0JfirDsbp_zfeDXoennVdM8YaXgD7X4AYnpaQsl64ZGEcjYewTLp8omqahnBVpPRTamNIKUL_8wwl-qMw_VuY_iisePb-5vtxfNfD3wBAKphs</recordid><startdate>20170620</startdate><enddate>20170620</enddate><creator>Oki, Shinya</creator><creator>Sone, Kenbun</creator><creator>Oda, Katsutoshi</creator><creator>Hamamoto, Ryuji</creator><creator>Ikemura, Masako</creator><creator>Maeda, Daichi</creator><creator>Takeuchi, Makoto</creator><creator>Tanikawa, Michihiro</creator><creator>Mori-Uchino, Mayuyo</creator><creator>Nagasaka, Kazunori</creator><creator>Miyasaka, Aki</creator><creator>Kashiyama, Tomoko</creator><creator>Ikeda, Yuji</creator><creator>Arimoto, Takahide</creator><creator>Kuramoto, Hiroyuki</creator><creator>Wada-Hiraike, Osamu</creator><creator>Kawana, Kei</creator><creator>Fukayama, Masashi</creator><creator>Osuga, Yutaka</creator><creator>Fujii, Tomoyuki</creator><general>Impact Journals LLC</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>7X8</scope><scope>5PM</scope></search><sort><creationdate>20170620</creationdate><title>Oncogenic histone methyltransferase EZH2: A novel prognostic marker with therapeutic potential in endometrial cancer</title><author>Oki, Shinya ; Sone, Kenbun ; Oda, Katsutoshi ; Hamamoto, Ryuji ; Ikemura, Masako ; Maeda, Daichi ; Takeuchi, Makoto ; Tanikawa, Michihiro ; Mori-Uchino, Mayuyo ; Nagasaka, Kazunori ; Miyasaka, Aki ; Kashiyama, Tomoko ; Ikeda, Yuji ; Arimoto, Takahide ; Kuramoto, Hiroyuki ; Wada-Hiraike, Osamu ; Kawana, Kei ; Fukayama, Masashi ; Osuga, Yutaka ; Fujii, Tomoyuki</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c400t-1d6a82e5027c2368e00a66c596ad9bb01b4d2fe83d285f68fe62b2edb8bc799c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Antineoplastic Agents - pharmacology</topic><topic>Antineoplastic Combined Chemotherapy Protocols - pharmacology</topic><topic>Apoptosis - drug effects</topic><topic>Apoptosis - genetics</topic><topic>Biomarkers, Tumor - genetics</topic><topic>Carcinogenesis - drug effects</topic><topic>Carcinogenesis - genetics</topic><topic>Cell Line, Tumor</topic><topic>Cell Proliferation - drug effects</topic><topic>Cell Proliferation - genetics</topic><topic>Cisplatin - pharmacology</topic><topic>Doxorubicin - pharmacology</topic><topic>Endometrial Neoplasms - drug therapy</topic><topic>Endometrial Neoplasms - genetics</topic><topic>Endometrial Neoplasms - mortality</topic><topic>Enhancer of Zeste Homolog 2 Protein - antagonists & inhibitors</topic><topic>Enhancer of Zeste Homolog 2 Protein - genetics</topic><topic>Enhancer of Zeste Homolog 2 Protein - metabolism</topic><topic>Female</topic><topic>Genetic Markers - genetics</topic><topic>Histones - metabolism</topic><topic>Humans</topic><topic>Indoles - pharmacology</topic><topic>Prognosis</topic><topic>Pyridones - pharmacology</topic><topic>Research Paper</topic><topic>RNA Interference</topic><topic>RNA, Small Interfering - genetics</topic><toplevel>online_resources</toplevel><creatorcontrib>Oki, Shinya</creatorcontrib><creatorcontrib>Sone, Kenbun</creatorcontrib><creatorcontrib>Oda, Katsutoshi</creatorcontrib><creatorcontrib>Hamamoto, Ryuji</creatorcontrib><creatorcontrib>Ikemura, Masako</creatorcontrib><creatorcontrib>Maeda, Daichi</creatorcontrib><creatorcontrib>Takeuchi, Makoto</creatorcontrib><creatorcontrib>Tanikawa, Michihiro</creatorcontrib><creatorcontrib>Mori-Uchino, Mayuyo</creatorcontrib><creatorcontrib>Nagasaka, Kazunori</creatorcontrib><creatorcontrib>Miyasaka, Aki</creatorcontrib><creatorcontrib>Kashiyama, Tomoko</creatorcontrib><creatorcontrib>Ikeda, Yuji</creatorcontrib><creatorcontrib>Arimoto, Takahide</creatorcontrib><creatorcontrib>Kuramoto, Hiroyuki</creatorcontrib><creatorcontrib>Wada-Hiraike, Osamu</creatorcontrib><creatorcontrib>Kawana, Kei</creatorcontrib><creatorcontrib>Fukayama, Masashi</creatorcontrib><creatorcontrib>Osuga, Yutaka</creatorcontrib><creatorcontrib>Fujii, Tomoyuki</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Oncotarget</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Oki, Shinya</au><au>Sone, Kenbun</au><au>Oda, Katsutoshi</au><au>Hamamoto, Ryuji</au><au>Ikemura, Masako</au><au>Maeda, Daichi</au><au>Takeuchi, Makoto</au><au>Tanikawa, Michihiro</au><au>Mori-Uchino, Mayuyo</au><au>Nagasaka, Kazunori</au><au>Miyasaka, Aki</au><au>Kashiyama, Tomoko</au><au>Ikeda, Yuji</au><au>Arimoto, Takahide</au><au>Kuramoto, Hiroyuki</au><au>Wada-Hiraike, Osamu</au><au>Kawana, Kei</au><au>Fukayama, Masashi</au><au>Osuga, Yutaka</au><au>Fujii, Tomoyuki</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Oncogenic histone methyltransferase EZH2: A novel prognostic marker with therapeutic potential in endometrial cancer</atitle><jtitle>Oncotarget</jtitle><addtitle>Oncotarget</addtitle><date>2017-06-20</date><risdate>2017</risdate><volume>8</volume><issue>25</issue><spage>40402</spage><epage>40411</epage><pages>40402-40411</pages><issn>1949-2553</issn><eissn>1949-2553</eissn><abstract>The histone methyltransferase EZH2, a key epigenetic modifier, is known to be associated with human tumorigenesis. However, the physiological importance of EZH2 and its clinical relevance in endometrial cancer remain unclear. Hence, in the present study, we investigated the expression and function of EZH2 in endometrial cancer. In a quantitative real-time PCR analysis of 11 endometrial cancer cell lines and 52 clinical endometrial cancer specimens, EZH2 was significantly overexpressed in cancer cells and tissues compared to that in corresponding normal control cells and tissues. Kaplan-Meier survival analysis using data of the TCGA RNA-seq database and tissue microarrays (TMAs) indicated that EZH2 overexpression is associated with endometrial cancer prognosis. In addition, knockdown of EZH2 using specific siRNAs resulted in growth suppression and apoptosis induction of endometrial cancer cells, accompanied by attenuation of H3K27 trimethylation. Consistent with these results, treatment with GSK126, a specific EZH2 inhibitor, suppressed endometrial cancer cell growth and decreased the number of cancer cell colonies. Furthermore, GSK126 showed additive effects with doxorubicin or cisplatin, which are conventional drugs for treatment of endometrial cancer. Further studies should explore the therapeutic potential of inhibiting EZH2 in patients with endometrial cancer.</abstract><cop>United States</cop><pub>Impact Journals LLC</pub><pmid>28418882</pmid><doi>10.18632/oncotarget.16316</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Antineoplastic Agents - pharmacology Antineoplastic Combined Chemotherapy Protocols - pharmacology Apoptosis - drug effects Apoptosis - genetics Biomarkers, Tumor - genetics Carcinogenesis - drug effects Carcinogenesis - genetics Cell Line, Tumor Cell Proliferation - drug effects Cell Proliferation - genetics Cisplatin - pharmacology Doxorubicin - pharmacology Endometrial Neoplasms - drug therapy Endometrial Neoplasms - genetics Endometrial Neoplasms - mortality Enhancer of Zeste Homolog 2 Protein - antagonists & inhibitors Enhancer of Zeste Homolog 2 Protein - genetics Enhancer of Zeste Homolog 2 Protein - metabolism Female Genetic Markers - genetics Histones - metabolism Humans Indoles - pharmacology Prognosis Pyridones - pharmacology Research Paper RNA Interference RNA, Small Interfering - genetics |
| title | Oncogenic histone methyltransferase EZH2: A novel prognostic marker with therapeutic potential in endometrial cancer |
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