Genome-wide CRISPR-Cas9 screen identified KLF11 as a druggable suppressor for sarcoma cancer stem cells
Cancer stem cells (CSCs) are involved in tumorigenesis, recurrence, and therapy resistance. To identify critical regulators of sarcoma CSCs, we performed a reporter-based genome-wide CRISPR-Cas9 screen and uncovered Kruppel-like factor 11 (KLF11) as top candidate. In vitro and in vivo functional ann...
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| Veröffentlicht in: | Science advances 2021-01, Vol.7 (5) |
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| creator | Wang, Yicun Wu, Jinhui Chen, Hui Yang, Yang Xiao, Chengwu Yi, Xiaoming Shi, Changjie Zhong, Ke He, Haowei Li, Yaoming Wu, Zhenjie Zhou, Guangxin Rao, Qiu Wang, Xiaoxia Zhou, Xiaodie Lomberk, Gwen Liu, Bing Zhao, Jianning Ge, Jingping Zhou, Wenquan Chu, Xiaoyuan Chen, Cheng Zhou, Xuhui Wang, Linhui Guan, Kunliang Qu, Le |
| description | Cancer stem cells (CSCs) are involved in tumorigenesis, recurrence, and therapy resistance. To identify critical regulators of sarcoma CSCs, we performed a reporter-based genome-wide CRISPR-Cas9 screen and uncovered Kruppel-like factor 11 (KLF11) as top candidate. In vitro and in vivo functional annotation defined a negative role of KLF11 in CSCs. Mechanistically, KLF11 and YAP/TEAD bound to adjacent DNA sites along with direct interaction. KLF11 recruited SIN3A/HDAC to suppress the transcriptional output of YAP/TEAD, which, in turn, promoted KLF11 transcription, forming a negative feedback loop. However, in CSCs, this negative feedback was lost because of epigenetic silence of KLF11, causing sustained YAP activation. Low KLF11 was associated with poor prognosis and chemotherapy response in patients with sarcoma. Pharmacological activation of KLF11 by thiazolidinedione effectively restored chemotherapy response. Collectively, our study identifies KLF11 as a negative regulator in sarcoma CSCs and potential therapeutic target. |
| doi_str_mv | 10.1126/sciadv.abe3445 |
| format | Article |
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To identify critical regulators of sarcoma CSCs, we performed a reporter-based genome-wide CRISPR-Cas9 screen and uncovered Kruppel-like factor 11 (KLF11) as top candidate. In vitro and in vivo functional annotation defined a negative role of KLF11 in CSCs. Mechanistically, KLF11 and YAP/TEAD bound to adjacent DNA sites along with direct interaction. KLF11 recruited SIN3A/HDAC to suppress the transcriptional output of YAP/TEAD, which, in turn, promoted KLF11 transcription, forming a negative feedback loop. However, in CSCs, this negative feedback was lost because of epigenetic silence of KLF11, causing sustained YAP activation. Low KLF11 was associated with poor prognosis and chemotherapy response in patients with sarcoma. Pharmacological activation of KLF11 by thiazolidinedione effectively restored chemotherapy response. Collectively, our study identifies KLF11 as a negative regulator in sarcoma CSCs and potential therapeutic target.</description><identifier>ISSN: 2375-2548</identifier><identifier>EISSN: 2375-2548</identifier><identifier>DOI: 10.1126/sciadv.abe3445</identifier><identifier>PMID: 33571129</identifier><language>eng</language><publisher>United States: American Association for the Advancement of Science</publisher><subject>Apoptosis Regulatory Proteins - metabolism ; Cancer ; Cell Biology ; CRISPR-Cas Systems - genetics ; Humans ; Neoplastic Stem Cells - metabolism ; Repressor Proteins - metabolism ; Sarcoma - drug therapy ; Sarcoma - genetics ; SciAdv r-articles</subject><ispartof>Science advances, 2021-01, Vol.7 (5)</ispartof><rights>Copyright © 2021 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works. Distributed under a Creative Commons Attribution NonCommercial License 4.0 (CC BY-NC).</rights><rights>Copyright © 2021 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works. Distributed under a Creative Commons Attribution NonCommercial License 4.0 (CC BY-NC). 2021 The Authors</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c390t-f46a358e35effd301a78c6144d0a07c3754d8ca9395d97287d25014815c674303</citedby><cites>FETCH-LOGICAL-c390t-f46a358e35effd301a78c6144d0a07c3754d8ca9395d97287d25014815c674303</cites><orcidid>0000-0001-9887-0685 ; 0000-0002-8026-5468 ; 0000-0003-4067-1637 ; 0000-0002-6487-5207 ; 0000-0002-0358-4983 ; 0000-0002-7917-7874 ; 0000-0003-1892-0174 ; 0000-0002-7901-0759 ; 0000-0002-1013-0429 ; 0000-0002-4056-0462 ; 0000-0002-4464-3230 ; 0000-0001-9499-4277 ; 0000-0002-5519-9235 ; 0000-0001-7158-2296 ; 0000-0001-6405-7733</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/PMC7840125/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7840125/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,724,777,781,861,882,27905,27906,53772,53774</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/33571129$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wang, Yicun</creatorcontrib><creatorcontrib>Wu, Jinhui</creatorcontrib><creatorcontrib>Chen, Hui</creatorcontrib><creatorcontrib>Yang, Yang</creatorcontrib><creatorcontrib>Xiao, Chengwu</creatorcontrib><creatorcontrib>Yi, Xiaoming</creatorcontrib><creatorcontrib>Shi, Changjie</creatorcontrib><creatorcontrib>Zhong, Ke</creatorcontrib><creatorcontrib>He, Haowei</creatorcontrib><creatorcontrib>Li, Yaoming</creatorcontrib><creatorcontrib>Wu, Zhenjie</creatorcontrib><creatorcontrib>Zhou, Guangxin</creatorcontrib><creatorcontrib>Rao, Qiu</creatorcontrib><creatorcontrib>Wang, Xiaoxia</creatorcontrib><creatorcontrib>Zhou, Xiaodie</creatorcontrib><creatorcontrib>Lomberk, Gwen</creatorcontrib><creatorcontrib>Liu, Bing</creatorcontrib><creatorcontrib>Zhao, Jianning</creatorcontrib><creatorcontrib>Ge, Jingping</creatorcontrib><creatorcontrib>Zhou, Wenquan</creatorcontrib><creatorcontrib>Chu, Xiaoyuan</creatorcontrib><creatorcontrib>Chen, Cheng</creatorcontrib><creatorcontrib>Zhou, Xuhui</creatorcontrib><creatorcontrib>Wang, Linhui</creatorcontrib><creatorcontrib>Guan, Kunliang</creatorcontrib><creatorcontrib>Qu, Le</creatorcontrib><title>Genome-wide CRISPR-Cas9 screen identified KLF11 as a druggable suppressor for sarcoma cancer stem cells</title><title>Science advances</title><addtitle>Sci Adv</addtitle><description>Cancer stem cells (CSCs) are involved in tumorigenesis, recurrence, and therapy resistance. To identify critical regulators of sarcoma CSCs, we performed a reporter-based genome-wide CRISPR-Cas9 screen and uncovered Kruppel-like factor 11 (KLF11) as top candidate. In vitro and in vivo functional annotation defined a negative role of KLF11 in CSCs. Mechanistically, KLF11 and YAP/TEAD bound to adjacent DNA sites along with direct interaction. KLF11 recruited SIN3A/HDAC to suppress the transcriptional output of YAP/TEAD, which, in turn, promoted KLF11 transcription, forming a negative feedback loop. However, in CSCs, this negative feedback was lost because of epigenetic silence of KLF11, causing sustained YAP activation. Low KLF11 was associated with poor prognosis and chemotherapy response in patients with sarcoma. Pharmacological activation of KLF11 by thiazolidinedione effectively restored chemotherapy response. Collectively, our study identifies KLF11 as a negative regulator in sarcoma CSCs and potential therapeutic target.</description><subject>Apoptosis Regulatory Proteins - metabolism</subject><subject>Cancer</subject><subject>Cell Biology</subject><subject>CRISPR-Cas Systems - genetics</subject><subject>Humans</subject><subject>Neoplastic Stem Cells - metabolism</subject><subject>Repressor Proteins - metabolism</subject><subject>Sarcoma - drug therapy</subject><subject>Sarcoma - genetics</subject><subject>SciAdv r-articles</subject><issn>2375-2548</issn><issn>2375-2548</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpVUU1PGzEQtVARIODaY-VjLxvstb32XipVUQmISKBAz9bEnk232o_UkwX139coAdHDaMae5-f39Bj7LMVMyrK6otBCfJ7BGpXW5oidlcqaojTaffown7JLot9CCKmrysj6hJ0qZWxmqM_YZoHD2GPx0kbk89Xt48OqmAPVnEJCHHi-HnZt02Lkd8trKTkQBx7TtNnAukNO03abkGhMvMlFkMLYAw8wBMzHHfY8YNfRBTtuoCO8PPRz9vP6x9P8pljeL27n35dFULXYFY2uQBmHymDTRCUkWBcqqXUUIGzIlnR0AWpVm1jb0tlYmuzLSRMqq5VQ5-zbnnc7rXuMIatP0PltantIf_0Irf9_M7S__GZ89tZpIUuTCb4eCNL4Z0La-b6lVwsw4DiRL7WrS22lchk620NDGokSNu_fSOFfA_L7gPwhoPzgy0dx7_C3ONQ_W9CNfQ</recordid><startdate>20210101</startdate><enddate>20210101</enddate><creator>Wang, Yicun</creator><creator>Wu, Jinhui</creator><creator>Chen, Hui</creator><creator>Yang, Yang</creator><creator>Xiao, Chengwu</creator><creator>Yi, Xiaoming</creator><creator>Shi, Changjie</creator><creator>Zhong, Ke</creator><creator>He, Haowei</creator><creator>Li, Yaoming</creator><creator>Wu, Zhenjie</creator><creator>Zhou, Guangxin</creator><creator>Rao, Qiu</creator><creator>Wang, Xiaoxia</creator><creator>Zhou, Xiaodie</creator><creator>Lomberk, Gwen</creator><creator>Liu, Bing</creator><creator>Zhao, Jianning</creator><creator>Ge, Jingping</creator><creator>Zhou, Wenquan</creator><creator>Chu, Xiaoyuan</creator><creator>Chen, Cheng</creator><creator>Zhou, Xuhui</creator><creator>Wang, Linhui</creator><creator>Guan, Kunliang</creator><creator>Qu, Le</creator><general>American Association for the Advancement of Science</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><orcidid>https://orcid.org/0000-0001-9887-0685</orcidid><orcidid>https://orcid.org/0000-0002-8026-5468</orcidid><orcidid>https://orcid.org/0000-0003-4067-1637</orcidid><orcidid>https://orcid.org/0000-0002-6487-5207</orcidid><orcidid>https://orcid.org/0000-0002-0358-4983</orcidid><orcidid>https://orcid.org/0000-0002-7917-7874</orcidid><orcidid>https://orcid.org/0000-0003-1892-0174</orcidid><orcidid>https://orcid.org/0000-0002-7901-0759</orcidid><orcidid>https://orcid.org/0000-0002-1013-0429</orcidid><orcidid>https://orcid.org/0000-0002-4056-0462</orcidid><orcidid>https://orcid.org/0000-0002-4464-3230</orcidid><orcidid>https://orcid.org/0000-0001-9499-4277</orcidid><orcidid>https://orcid.org/0000-0002-5519-9235</orcidid><orcidid>https://orcid.org/0000-0001-7158-2296</orcidid><orcidid>https://orcid.org/0000-0001-6405-7733</orcidid></search><sort><creationdate>20210101</creationdate><title>Genome-wide CRISPR-Cas9 screen identified KLF11 as a druggable suppressor for sarcoma cancer stem cells</title><author>Wang, Yicun ; Wu, Jinhui ; Chen, Hui ; Yang, Yang ; Xiao, Chengwu ; Yi, Xiaoming ; Shi, Changjie ; Zhong, Ke ; He, Haowei ; Li, Yaoming ; Wu, Zhenjie ; Zhou, Guangxin ; Rao, Qiu ; Wang, Xiaoxia ; Zhou, Xiaodie ; Lomberk, Gwen ; Liu, Bing ; Zhao, Jianning ; Ge, Jingping ; Zhou, Wenquan ; Chu, Xiaoyuan ; Chen, Cheng ; Zhou, Xuhui ; Wang, Linhui ; Guan, Kunliang ; Qu, Le</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c390t-f46a358e35effd301a78c6144d0a07c3754d8ca9395d97287d25014815c674303</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Apoptosis Regulatory Proteins - metabolism</topic><topic>Cancer</topic><topic>Cell Biology</topic><topic>CRISPR-Cas Systems - genetics</topic><topic>Humans</topic><topic>Neoplastic Stem Cells - metabolism</topic><topic>Repressor Proteins - metabolism</topic><topic>Sarcoma - drug therapy</topic><topic>Sarcoma - genetics</topic><topic>SciAdv r-articles</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wang, Yicun</creatorcontrib><creatorcontrib>Wu, Jinhui</creatorcontrib><creatorcontrib>Chen, Hui</creatorcontrib><creatorcontrib>Yang, Yang</creatorcontrib><creatorcontrib>Xiao, Chengwu</creatorcontrib><creatorcontrib>Yi, Xiaoming</creatorcontrib><creatorcontrib>Shi, Changjie</creatorcontrib><creatorcontrib>Zhong, Ke</creatorcontrib><creatorcontrib>He, Haowei</creatorcontrib><creatorcontrib>Li, Yaoming</creatorcontrib><creatorcontrib>Wu, Zhenjie</creatorcontrib><creatorcontrib>Zhou, Guangxin</creatorcontrib><creatorcontrib>Rao, Qiu</creatorcontrib><creatorcontrib>Wang, Xiaoxia</creatorcontrib><creatorcontrib>Zhou, Xiaodie</creatorcontrib><creatorcontrib>Lomberk, Gwen</creatorcontrib><creatorcontrib>Liu, Bing</creatorcontrib><creatorcontrib>Zhao, Jianning</creatorcontrib><creatorcontrib>Ge, Jingping</creatorcontrib><creatorcontrib>Zhou, Wenquan</creatorcontrib><creatorcontrib>Chu, Xiaoyuan</creatorcontrib><creatorcontrib>Chen, Cheng</creatorcontrib><creatorcontrib>Zhou, Xuhui</creatorcontrib><creatorcontrib>Wang, Linhui</creatorcontrib><creatorcontrib>Guan, Kunliang</creatorcontrib><creatorcontrib>Qu, Le</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>Science advances</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wang, Yicun</au><au>Wu, Jinhui</au><au>Chen, Hui</au><au>Yang, Yang</au><au>Xiao, Chengwu</au><au>Yi, Xiaoming</au><au>Shi, Changjie</au><au>Zhong, Ke</au><au>He, Haowei</au><au>Li, Yaoming</au><au>Wu, Zhenjie</au><au>Zhou, Guangxin</au><au>Rao, Qiu</au><au>Wang, Xiaoxia</au><au>Zhou, Xiaodie</au><au>Lomberk, Gwen</au><au>Liu, Bing</au><au>Zhao, Jianning</au><au>Ge, Jingping</au><au>Zhou, Wenquan</au><au>Chu, Xiaoyuan</au><au>Chen, Cheng</au><au>Zhou, Xuhui</au><au>Wang, Linhui</au><au>Guan, Kunliang</au><au>Qu, Le</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Genome-wide CRISPR-Cas9 screen identified KLF11 as a druggable suppressor for sarcoma cancer stem cells</atitle><jtitle>Science advances</jtitle><addtitle>Sci Adv</addtitle><date>2021-01-01</date><risdate>2021</risdate><volume>7</volume><issue>5</issue><issn>2375-2548</issn><eissn>2375-2548</eissn><abstract>Cancer stem cells (CSCs) are involved in tumorigenesis, recurrence, and therapy resistance. To identify critical regulators of sarcoma CSCs, we performed a reporter-based genome-wide CRISPR-Cas9 screen and uncovered Kruppel-like factor 11 (KLF11) as top candidate. In vitro and in vivo functional annotation defined a negative role of KLF11 in CSCs. Mechanistically, KLF11 and YAP/TEAD bound to adjacent DNA sites along with direct interaction. KLF11 recruited SIN3A/HDAC to suppress the transcriptional output of YAP/TEAD, which, in turn, promoted KLF11 transcription, forming a negative feedback loop. However, in CSCs, this negative feedback was lost because of epigenetic silence of KLF11, causing sustained YAP activation. Low KLF11 was associated with poor prognosis and chemotherapy response in patients with sarcoma. Pharmacological activation of KLF11 by thiazolidinedione effectively restored chemotherapy response. 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| subjects | Apoptosis Regulatory Proteins - metabolism Cancer Cell Biology CRISPR-Cas Systems - genetics Humans Neoplastic Stem Cells - metabolism Repressor Proteins - metabolism Sarcoma - drug therapy Sarcoma - genetics SciAdv r-articles |
| title | Genome-wide CRISPR-Cas9 screen identified KLF11 as a druggable suppressor for sarcoma cancer stem cells |
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