Polycomb-like 2 regulates PRC2 components to affect proliferation in glioma cells
Introduction The Polycomb group (PcG) is an important family of transcriptional regulators that controls growth and tumorigenesis. The PcG mainly consists of two complexes, PRC1 and Polycomb Repressive Complex 2 (PRC2). Polycomb-like 2 (PCL2) is known to interact with the PRC2 protein. The role of P...
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| Veröffentlicht in: | Journal of neuro-oncology 2020-06, Vol.148 (2), p.259-271 |
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| description | Introduction
The Polycomb group (PcG) is an important family of transcriptional regulators that controls growth and tumorigenesis. The PcG mainly consists of two complexes, PRC1 and Polycomb Repressive Complex 2 (PRC2). Polycomb-like 2 (PCL2) is known to interact with the PRC2 protein. The role of PCL2 in the development and progression of glioma is unclear.
Methods
We use The Cancer Genome Atlas (TCGA) database to detect the expression of PCL2 in various tumors. 117 cases of clinical glioma (WHOI–IV) were collected, and PCL2 expression and localization were detected by immunohistochemical staining. Glioma cells U87/U251 were infected with overexpressed and interfered PCL2. CCK8 assay, colony formation assay, EdU method, cell cycle and apoptosis were used to detect cell proliferation and apoptosis. Western blot was used to detect the expression of PRC2-related core proteins. After DZNeP intervention, PRC2 protein expression was again measured to discuss the mechanism of PCL2 action.
Results
TCGA database results and immunohistochemical staining results suggest that PCL2 is highly expressed in gliomas. We found that the PCL2 gene promoted tumor cell proliferation, enhanced the colony formation ability, and increased S phase in the cell cycle. The overexpression of PCL2 upregulated the expression levels of EZH2 and EED (two core members of PRC2), decreased the expression of SUZ12, increased the level of H3K27 trimethylation (H3K27me3), H3K4 dimethylation (H3K4me2), and decreased H3K9 dimethylation (H3K9me2). The result after interfering with PCL2 was the opposite.
Conclusions
As an important accessory protein of PRC2, PCL2 can not only change the expression of PRC2 components, but also affect the expression level of Histone methylation. Therefore, PCL2 may be an important hub for regulating the synergy among PRC2 members. This study revealed PCL2 as a new target for tumor research and open up a new avenue for future research in glioma. |
| doi_str_mv | 10.1007/s11060-020-03538-0 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_7316845</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2405336364</sourcerecordid><originalsourceid>FETCH-LOGICAL-c474t-7ff7cdd049b625a62a7376e0a813c866f1c355ba1aa41c0618204a89f0865b2c3</originalsourceid><addsrcrecordid>eNp9kUuLFDEUhYMoTtv6B1xIwI2b0nvzrN4I0viCAUdRcBdS6aTNmKq0SZUw_960PY6PhYski_vl5JwcQh4iPEUA_awigoIOWFtc8r6DW2SFUvNOc81vkxWg0p3ciM9n5F6tlwAgNMe75IwzwRWiXpH3FzlduTwOXYpfPWW0-P2S7OwrvfiwZbSNDnny01zpnKkNwbuZHkpOMfhi55gnGie6TzGPljqfUr1P7gSbqn9wfa7Jp1cvP27fdOfvXr_dvjjvnNBi7nQI2u12IDaDYtIqZptp5cH2yF2vVEDHpRwsWivQgcKegbD9JkCv5MAcX5PnJ93DMox-55rHYpM5lDjacmWyjebvyRS_mH3-btoXqF7IJvDkWqDkb4uvsxljPUawk89LNUyA5FxxJRr6-B_0Mi9lavEahRqVOoJrwk6UK7nW4sONGQRzbMycGjOtMfOzsbavyaM_Y9xc-VVRA_gJqG007X35_fZ_ZH8AzMeg2Q</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2417166336</pqid></control><display><type>article</type><title>Polycomb-like 2 regulates PRC2 components to affect proliferation in glioma cells</title><source>MEDLINE</source><source>Springer Nature - Complete Springer Journals</source><creator>Wang, Fei ; Gao, Yongying ; Lv, Ye ; Wu, Yanwei ; Guo, Yongzhen ; Du, Fang ; Wang, Shixiong ; Yu, Jiaxiang ; Cao, Xiangmei ; Li, P. Andy</creator><creatorcontrib>Wang, Fei ; Gao, Yongying ; Lv, Ye ; Wu, Yanwei ; Guo, Yongzhen ; Du, Fang ; Wang, Shixiong ; Yu, Jiaxiang ; Cao, Xiangmei ; Li, P. Andy</creatorcontrib><description>Introduction
The Polycomb group (PcG) is an important family of transcriptional regulators that controls growth and tumorigenesis. The PcG mainly consists of two complexes, PRC1 and Polycomb Repressive Complex 2 (PRC2). Polycomb-like 2 (PCL2) is known to interact with the PRC2 protein. The role of PCL2 in the development and progression of glioma is unclear.
Methods
We use The Cancer Genome Atlas (TCGA) database to detect the expression of PCL2 in various tumors. 117 cases of clinical glioma (WHOI–IV) were collected, and PCL2 expression and localization were detected by immunohistochemical staining. Glioma cells U87/U251 were infected with overexpressed and interfered PCL2. CCK8 assay, colony formation assay, EdU method, cell cycle and apoptosis were used to detect cell proliferation and apoptosis. Western blot was used to detect the expression of PRC2-related core proteins. After DZNeP intervention, PRC2 protein expression was again measured to discuss the mechanism of PCL2 action.
Results
TCGA database results and immunohistochemical staining results suggest that PCL2 is highly expressed in gliomas. We found that the PCL2 gene promoted tumor cell proliferation, enhanced the colony formation ability, and increased S phase in the cell cycle. The overexpression of PCL2 upregulated the expression levels of EZH2 and EED (two core members of PRC2), decreased the expression of SUZ12, increased the level of H3K27 trimethylation (H3K27me3), H3K4 dimethylation (H3K4me2), and decreased H3K9 dimethylation (H3K9me2). The result after interfering with PCL2 was the opposite.
Conclusions
As an important accessory protein of PRC2, PCL2 can not only change the expression of PRC2 components, but also affect the expression level of Histone methylation. Therefore, PCL2 may be an important hub for regulating the synergy among PRC2 members. This study revealed PCL2 as a new target for tumor research and open up a new avenue for future research in glioma.</description><identifier>ISSN: 0167-594X</identifier><identifier>EISSN: 1573-7373</identifier><identifier>DOI: 10.1007/s11060-020-03538-0</identifier><identifier>PMID: 32436117</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Apoptosis ; Brain Neoplasms - metabolism ; Brain tumors ; Cell cycle ; Cell growth ; Cell Line, Tumor ; Cell Proliferation ; Colonies ; Genomes ; Glioma ; Glioma - metabolism ; Glioma cells ; Histones - metabolism ; Humans ; Laboratory Investigation ; Localization ; Medicine ; Medicine & Public Health ; Methylation ; Neurology ; Oncology ; Polycomb group proteins ; Polycomb Repressive Complex 2 - metabolism ; Proteins ; S phase ; Transcription ; Tumorigenesis</subject><ispartof>Journal of neuro-oncology, 2020-06, Vol.148 (2), p.259-271</ispartof><rights>The Author(s) 2020</rights><rights>The Author(s) 2020. This work is published under http://creativecommons.org/licenses/by/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-c474t-7ff7cdd049b625a62a7376e0a813c866f1c355ba1aa41c0618204a89f0865b2c3</citedby><cites>FETCH-LOGICAL-c474t-7ff7cdd049b625a62a7376e0a813c866f1c355ba1aa41c0618204a89f0865b2c3</cites><orcidid>0000-0003-4719-2233</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s11060-020-03538-0$$EPDF$$P50$$Gspringer$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s11060-020-03538-0$$EHTML$$P50$$Gspringer$$Hfree_for_read</linktohtml><link.rule.ids>230,314,776,780,881,27903,27904,41467,42536,51297</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32436117$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wang, Fei</creatorcontrib><creatorcontrib>Gao, Yongying</creatorcontrib><creatorcontrib>Lv, Ye</creatorcontrib><creatorcontrib>Wu, Yanwei</creatorcontrib><creatorcontrib>Guo, Yongzhen</creatorcontrib><creatorcontrib>Du, Fang</creatorcontrib><creatorcontrib>Wang, Shixiong</creatorcontrib><creatorcontrib>Yu, Jiaxiang</creatorcontrib><creatorcontrib>Cao, Xiangmei</creatorcontrib><creatorcontrib>Li, P. Andy</creatorcontrib><title>Polycomb-like 2 regulates PRC2 components to affect proliferation in glioma cells</title><title>Journal of neuro-oncology</title><addtitle>J Neurooncol</addtitle><addtitle>J Neurooncol</addtitle><description>Introduction
The Polycomb group (PcG) is an important family of transcriptional regulators that controls growth and tumorigenesis. The PcG mainly consists of two complexes, PRC1 and Polycomb Repressive Complex 2 (PRC2). Polycomb-like 2 (PCL2) is known to interact with the PRC2 protein. The role of PCL2 in the development and progression of glioma is unclear.
Methods
We use The Cancer Genome Atlas (TCGA) database to detect the expression of PCL2 in various tumors. 117 cases of clinical glioma (WHOI–IV) were collected, and PCL2 expression and localization were detected by immunohistochemical staining. Glioma cells U87/U251 were infected with overexpressed and interfered PCL2. CCK8 assay, colony formation assay, EdU method, cell cycle and apoptosis were used to detect cell proliferation and apoptosis. Western blot was used to detect the expression of PRC2-related core proteins. After DZNeP intervention, PRC2 protein expression was again measured to discuss the mechanism of PCL2 action.
Results
TCGA database results and immunohistochemical staining results suggest that PCL2 is highly expressed in gliomas. We found that the PCL2 gene promoted tumor cell proliferation, enhanced the colony formation ability, and increased S phase in the cell cycle. The overexpression of PCL2 upregulated the expression levels of EZH2 and EED (two core members of PRC2), decreased the expression of SUZ12, increased the level of H3K27 trimethylation (H3K27me3), H3K4 dimethylation (H3K4me2), and decreased H3K9 dimethylation (H3K9me2). The result after interfering with PCL2 was the opposite.
Conclusions
As an important accessory protein of PRC2, PCL2 can not only change the expression of PRC2 components, but also affect the expression level of Histone methylation. Therefore, PCL2 may be an important hub for regulating the synergy among PRC2 members. This study revealed PCL2 as a new target for tumor research and open up a new avenue for future research in glioma.</description><subject>Apoptosis</subject><subject>Brain Neoplasms - metabolism</subject><subject>Brain tumors</subject><subject>Cell cycle</subject><subject>Cell growth</subject><subject>Cell Line, Tumor</subject><subject>Cell Proliferation</subject><subject>Colonies</subject><subject>Genomes</subject><subject>Glioma</subject><subject>Glioma - metabolism</subject><subject>Glioma cells</subject><subject>Histones - metabolism</subject><subject>Humans</subject><subject>Laboratory Investigation</subject><subject>Localization</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Methylation</subject><subject>Neurology</subject><subject>Oncology</subject><subject>Polycomb group proteins</subject><subject>Polycomb Repressive Complex 2 - metabolism</subject><subject>Proteins</subject><subject>S phase</subject><subject>Transcription</subject><subject>Tumorigenesis</subject><issn>0167-594X</issn><issn>1573-7373</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>C6C</sourceid><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNp9kUuLFDEUhYMoTtv6B1xIwI2b0nvzrN4I0viCAUdRcBdS6aTNmKq0SZUw_960PY6PhYski_vl5JwcQh4iPEUA_awigoIOWFtc8r6DW2SFUvNOc81vkxWg0p3ciM9n5F6tlwAgNMe75IwzwRWiXpH3FzlduTwOXYpfPWW0-P2S7OwrvfiwZbSNDnny01zpnKkNwbuZHkpOMfhi55gnGie6TzGPljqfUr1P7gSbqn9wfa7Jp1cvP27fdOfvXr_dvjjvnNBi7nQI2u12IDaDYtIqZptp5cH2yF2vVEDHpRwsWivQgcKegbD9JkCv5MAcX5PnJ93DMox-55rHYpM5lDjacmWyjebvyRS_mH3-btoXqF7IJvDkWqDkb4uvsxljPUawk89LNUyA5FxxJRr6-B_0Mi9lavEahRqVOoJrwk6UK7nW4sONGQRzbMycGjOtMfOzsbavyaM_Y9xc-VVRA_gJqG007X35_fZ_ZH8AzMeg2Q</recordid><startdate>20200601</startdate><enddate>20200601</enddate><creator>Wang, Fei</creator><creator>Gao, Yongying</creator><creator>Lv, Ye</creator><creator>Wu, Yanwei</creator><creator>Guo, Yongzhen</creator><creator>Du, Fang</creator><creator>Wang, Shixiong</creator><creator>Yu, Jiaxiang</creator><creator>Cao, Xiangmei</creator><creator>Li, P. Andy</creator><general>Springer US</general><general>Springer Nature B.V</general><scope>C6C</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>3V.</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0003-4719-2233</orcidid></search><sort><creationdate>20200601</creationdate><title>Polycomb-like 2 regulates PRC2 components to affect proliferation in glioma cells</title><author>Wang, Fei ; Gao, Yongying ; Lv, Ye ; Wu, Yanwei ; Guo, Yongzhen ; Du, Fang ; Wang, Shixiong ; Yu, Jiaxiang ; Cao, Xiangmei ; Li, P. Andy</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c474t-7ff7cdd049b625a62a7376e0a813c866f1c355ba1aa41c0618204a89f0865b2c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Apoptosis</topic><topic>Brain Neoplasms - metabolism</topic><topic>Brain tumors</topic><topic>Cell cycle</topic><topic>Cell growth</topic><topic>Cell Line, Tumor</topic><topic>Cell Proliferation</topic><topic>Colonies</topic><topic>Genomes</topic><topic>Glioma</topic><topic>Glioma - metabolism</topic><topic>Glioma cells</topic><topic>Histones - metabolism</topic><topic>Humans</topic><topic>Laboratory Investigation</topic><topic>Localization</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Methylation</topic><topic>Neurology</topic><topic>Oncology</topic><topic>Polycomb group proteins</topic><topic>Polycomb Repressive Complex 2 - metabolism</topic><topic>Proteins</topic><topic>S phase</topic><topic>Transcription</topic><topic>Tumorigenesis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wang, Fei</creatorcontrib><creatorcontrib>Gao, Yongying</creatorcontrib><creatorcontrib>Lv, Ye</creatorcontrib><creatorcontrib>Wu, Yanwei</creatorcontrib><creatorcontrib>Guo, Yongzhen</creatorcontrib><creatorcontrib>Du, Fang</creatorcontrib><creatorcontrib>Wang, Shixiong</creatorcontrib><creatorcontrib>Yu, Jiaxiang</creatorcontrib><creatorcontrib>Cao, Xiangmei</creatorcontrib><creatorcontrib>Li, P. Andy</creatorcontrib><collection>Springer Nature OA Free Journals</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 Central (Corporate)</collection><collection>Neurosciences 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>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>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Journal of neuro-oncology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wang, Fei</au><au>Gao, Yongying</au><au>Lv, Ye</au><au>Wu, Yanwei</au><au>Guo, Yongzhen</au><au>Du, Fang</au><au>Wang, Shixiong</au><au>Yu, Jiaxiang</au><au>Cao, Xiangmei</au><au>Li, P. Andy</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Polycomb-like 2 regulates PRC2 components to affect proliferation in glioma cells</atitle><jtitle>Journal of neuro-oncology</jtitle><stitle>J Neurooncol</stitle><addtitle>J Neurooncol</addtitle><date>2020-06-01</date><risdate>2020</risdate><volume>148</volume><issue>2</issue><spage>259</spage><epage>271</epage><pages>259-271</pages><issn>0167-594X</issn><eissn>1573-7373</eissn><abstract>Introduction
The Polycomb group (PcG) is an important family of transcriptional regulators that controls growth and tumorigenesis. The PcG mainly consists of two complexes, PRC1 and Polycomb Repressive Complex 2 (PRC2). Polycomb-like 2 (PCL2) is known to interact with the PRC2 protein. The role of PCL2 in the development and progression of glioma is unclear.
Methods
We use The Cancer Genome Atlas (TCGA) database to detect the expression of PCL2 in various tumors. 117 cases of clinical glioma (WHOI–IV) were collected, and PCL2 expression and localization were detected by immunohistochemical staining. Glioma cells U87/U251 were infected with overexpressed and interfered PCL2. CCK8 assay, colony formation assay, EdU method, cell cycle and apoptosis were used to detect cell proliferation and apoptosis. Western blot was used to detect the expression of PRC2-related core proteins. After DZNeP intervention, PRC2 protein expression was again measured to discuss the mechanism of PCL2 action.
Results
TCGA database results and immunohistochemical staining results suggest that PCL2 is highly expressed in gliomas. We found that the PCL2 gene promoted tumor cell proliferation, enhanced the colony formation ability, and increased S phase in the cell cycle. The overexpression of PCL2 upregulated the expression levels of EZH2 and EED (two core members of PRC2), decreased the expression of SUZ12, increased the level of H3K27 trimethylation (H3K27me3), H3K4 dimethylation (H3K4me2), and decreased H3K9 dimethylation (H3K9me2). The result after interfering with PCL2 was the opposite.
Conclusions
As an important accessory protein of PRC2, PCL2 can not only change the expression of PRC2 components, but also affect the expression level of Histone methylation. Therefore, PCL2 may be an important hub for regulating the synergy among PRC2 members. This study revealed PCL2 as a new target for tumor research and open up a new avenue for future research in glioma.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>32436117</pmid><doi>10.1007/s11060-020-03538-0</doi><tpages>13</tpages><orcidid>https://orcid.org/0000-0003-4719-2233</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Apoptosis Brain Neoplasms - metabolism Brain tumors Cell cycle Cell growth Cell Line, Tumor Cell Proliferation Colonies Genomes Glioma Glioma - metabolism Glioma cells Histones - metabolism Humans Laboratory Investigation Localization Medicine Medicine & Public Health Methylation Neurology Oncology Polycomb group proteins Polycomb Repressive Complex 2 - metabolism Proteins S phase Transcription Tumorigenesis |
| title | Polycomb-like 2 regulates PRC2 components to affect proliferation in glioma cells |
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