QKI deficiency maintains glioma stem cell stemness by activating the SHH/GLI1 signaling pathway
Purpose Glioblastoma (GBM) stem cells (GSCs) have been found to be the main cause of malignant GBM progression. It has also been found that Quaking homolog (QKI ) plays a predominant role in driving GBM development. Here, we aimed to asses the role of QKI in maintaining GSC stemness and inducing the...
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| Veröffentlicht in: | Cellular oncology (Dordrecht) 2019-12, Vol.42 (6), p.801-813 |
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| container_title | Cellular oncology (Dordrecht) |
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| creator | Han, Bo Wang, Ruijia Chen, Yongjie Meng, Xiangqi Wu, Pengfei Li, Ziwei Duan, Chunbin Li, Qingbin Li, Yang Zhao, Shihong Jiang, Chuanlu Cai, Jinquan |
| description | Purpose
Glioblastoma (GBM) stem cells (GSCs) have been found to be the main cause of malignant GBM progression. It has also been found that Quaking homolog (QKI
)
plays a predominant role in driving GBM development. Here, we aimed to asses the role of QKI in maintaining GSC stemness and inducing the invasiveness of GBM cells.
Methods
Public databases were used to assess the expression of QKI and its correlation with stemness markers in primary GBMs. The CRISPR-Cas9 technology was used to generate
QK
I knockout GBM cells, and RNA immunoprecipitation was used to assess QKI-
GLI1
protein-mRNA interactions. In addition, in vitro and in vivo GBM cell proliferation, migration, xenografting and neurosphere formation assays were performed.
Results
Using public GBM databases, QKI was identified as a potential GSC regulator. We found that QKI could inhibit stem-like cell (SLC) stemness and prolong the survival of xenografted mice. Mechanistically, we found that
QKI
knockout increased the GLI Family Zinc Finger 1 (
GLI1
) mRNA level, which is essential for maintaining the self-renewal ability of GSCs. In addition, we found that
QKI
knockout activated the Hedgehog signaling pathway via Tra-2 and GLI response element (TGE)-specific
GLI1
mRNA disruption.
Conclusion
Our data indicate that upregulation of GLI1 induced by QKI deficiency maintains GSC stemness and enhances the invasiveness of GBM cells, thereby hinting at new options for the treatment of GBM. |
| doi_str_mv | 10.1007/s13402-019-00463-x |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_2256105641</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2256105641</sourcerecordid><originalsourceid>FETCH-LOGICAL-c375t-d7cb5932cd7f45ccaefe419b83bf0df7d585d8fe784dbaddfe6e4169e705f1173</originalsourceid><addsrcrecordid>eNp9kU1LAzEQhoMoKuof8CABL17W5mOT3T1K0bZYEFHPIZtMamQ_6mar7b83tbWCBwkhQ-aZd4Z5ETqn5JoSkg0C5SlhCaFFQkgqebLcQ8eMUZrwlMv9XczyI3QWwhsha4xKIQ_REaesiIccI_V4P8EWnDceGrPCtfZNH2_As8q3tcahhxobqKrvqIEQcLnC2vT-Q_e-meH-FfDTeDwYTScUBz9rdLX-nuv-9VOvTtGB01WAs-17gl7ubp-H42T6MJoMb6aJ4ZnoE5uZUhScGZu5VBijwUFKizLnpSPWZVbkwuYOsjy1pbbWgYx5WUBGhKM04yfoaqM779r3BYRe1T6sx9YNtIugGBOSEiFTGtHLP-hbu-ji2JHiVMblEiIixTaU6doQOnBq3vladytFiVo7oDYOqOiA-nZALWPRxVZ6UdZgdyU_-44A3wAhppoZdL-9_5H9AoWKkWU</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2316007005</pqid></control><display><type>article</type><title>QKI deficiency maintains glioma stem cell stemness by activating the SHH/GLI1 signaling pathway</title><source>MEDLINE</source><source>SpringerLink Journals - AutoHoldings</source><creator>Han, Bo ; Wang, Ruijia ; Chen, Yongjie ; Meng, Xiangqi ; Wu, Pengfei ; Li, Ziwei ; Duan, Chunbin ; Li, Qingbin ; Li, Yang ; Zhao, Shihong ; Jiang, Chuanlu ; Cai, Jinquan</creator><creatorcontrib>Han, Bo ; Wang, Ruijia ; Chen, Yongjie ; Meng, Xiangqi ; Wu, Pengfei ; Li, Ziwei ; Duan, Chunbin ; Li, Qingbin ; Li, Yang ; Zhao, Shihong ; Jiang, Chuanlu ; Cai, Jinquan</creatorcontrib><description>Purpose
Glioblastoma (GBM) stem cells (GSCs) have been found to be the main cause of malignant GBM progression. It has also been found that Quaking homolog (QKI
)
plays a predominant role in driving GBM development. Here, we aimed to asses the role of QKI in maintaining GSC stemness and inducing the invasiveness of GBM cells.
Methods
Public databases were used to assess the expression of QKI and its correlation with stemness markers in primary GBMs. The CRISPR-Cas9 technology was used to generate
QK
I knockout GBM cells, and RNA immunoprecipitation was used to assess QKI-
GLI1
protein-mRNA interactions. In addition, in vitro and in vivo GBM cell proliferation, migration, xenografting and neurosphere formation assays were performed.
Results
Using public GBM databases, QKI was identified as a potential GSC regulator. We found that QKI could inhibit stem-like cell (SLC) stemness and prolong the survival of xenografted mice. Mechanistically, we found that
QKI
knockout increased the GLI Family Zinc Finger 1 (
GLI1
) mRNA level, which is essential for maintaining the self-renewal ability of GSCs. In addition, we found that
QKI
knockout activated the Hedgehog signaling pathway via Tra-2 and GLI response element (TGE)-specific
GLI1
mRNA disruption.
Conclusion
Our data indicate that upregulation of GLI1 induced by QKI deficiency maintains GSC stemness and enhances the invasiveness of GBM cells, thereby hinting at new options for the treatment of GBM.</description><identifier>ISSN: 2211-3428</identifier><identifier>EISSN: 2211-3436</identifier><identifier>DOI: 10.1007/s13402-019-00463-x</identifier><identifier>PMID: 31292920</identifier><language>eng</language><publisher>Dordrecht: Springer Netherlands</publisher><subject>Aged ; Animals ; Biomedical and Life Sciences ; Biomedicine ; Brain Neoplasms - genetics ; Brain Neoplasms - metabolism ; Brain Neoplasms - pathology ; Cancer Research ; Cell Line, Tumor ; Cell migration ; Cell Proliferation ; Cell self-renewal ; CRISPR ; Female ; Gene Expression Regulation, Neoplastic ; Gli1 protein ; Glioblastoma ; Glioma - genetics ; Glioma - metabolism ; Glioma - pathology ; Glioma cells ; Hedgehog protein ; Hedgehog Proteins - metabolism ; Humans ; Immunoprecipitation ; Invasiveness ; Male ; Mice, Inbred BALB C ; Mice, Nude ; Middle Aged ; Models, Biological ; mRNA ; Neoplasm Invasiveness ; Neoplastic Stem Cells - metabolism ; Neoplastic Stem Cells - pathology ; Oncology ; Original Paper ; Pathology ; Phenotype ; Phosphorylation ; RNA, Messenger - genetics ; RNA, Messenger - metabolism ; RNA-Binding Proteins - genetics ; RNA-Binding Proteins - metabolism ; Signal Transduction ; Stem cell transplantation ; Stem cells ; Survival Analysis ; Xenografts ; Zinc Finger Protein GLI1 - metabolism ; Zinc finger proteins</subject><ispartof>Cellular oncology (Dordrecht), 2019-12, Vol.42 (6), p.801-813</ispartof><rights>International Society for Cellular Oncology 2019</rights><rights>Copyright Springer Nature B.V. 2019</rights><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c375t-d7cb5932cd7f45ccaefe419b83bf0df7d585d8fe784dbaddfe6e4169e705f1173</citedby><cites>FETCH-LOGICAL-c375t-d7cb5932cd7f45ccaefe419b83bf0df7d585d8fe784dbaddfe6e4169e705f1173</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s13402-019-00463-x$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s13402-019-00463-x$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>315,781,785,27926,27927,41490,42559,51321</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31292920$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Han, Bo</creatorcontrib><creatorcontrib>Wang, Ruijia</creatorcontrib><creatorcontrib>Chen, Yongjie</creatorcontrib><creatorcontrib>Meng, Xiangqi</creatorcontrib><creatorcontrib>Wu, Pengfei</creatorcontrib><creatorcontrib>Li, Ziwei</creatorcontrib><creatorcontrib>Duan, Chunbin</creatorcontrib><creatorcontrib>Li, Qingbin</creatorcontrib><creatorcontrib>Li, Yang</creatorcontrib><creatorcontrib>Zhao, Shihong</creatorcontrib><creatorcontrib>Jiang, Chuanlu</creatorcontrib><creatorcontrib>Cai, Jinquan</creatorcontrib><title>QKI deficiency maintains glioma stem cell stemness by activating the SHH/GLI1 signaling pathway</title><title>Cellular oncology (Dordrecht)</title><addtitle>Cell Oncol</addtitle><addtitle>Cell Oncol (Dordr)</addtitle><description>Purpose
Glioblastoma (GBM) stem cells (GSCs) have been found to be the main cause of malignant GBM progression. It has also been found that Quaking homolog (QKI
)
plays a predominant role in driving GBM development. Here, we aimed to asses the role of QKI in maintaining GSC stemness and inducing the invasiveness of GBM cells.
Methods
Public databases were used to assess the expression of QKI and its correlation with stemness markers in primary GBMs. The CRISPR-Cas9 technology was used to generate
QK
I knockout GBM cells, and RNA immunoprecipitation was used to assess QKI-
GLI1
protein-mRNA interactions. In addition, in vitro and in vivo GBM cell proliferation, migration, xenografting and neurosphere formation assays were performed.
Results
Using public GBM databases, QKI was identified as a potential GSC regulator. We found that QKI could inhibit stem-like cell (SLC) stemness and prolong the survival of xenografted mice. Mechanistically, we found that
QKI
knockout increased the GLI Family Zinc Finger 1 (
GLI1
) mRNA level, which is essential for maintaining the self-renewal ability of GSCs. In addition, we found that
QKI
knockout activated the Hedgehog signaling pathway via Tra-2 and GLI response element (TGE)-specific
GLI1
mRNA disruption.
Conclusion
Our data indicate that upregulation of GLI1 induced by QKI deficiency maintains GSC stemness and enhances the invasiveness of GBM cells, thereby hinting at new options for the treatment of GBM.</description><subject>Aged</subject><subject>Animals</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Brain Neoplasms - genetics</subject><subject>Brain Neoplasms - metabolism</subject><subject>Brain Neoplasms - pathology</subject><subject>Cancer Research</subject><subject>Cell Line, Tumor</subject><subject>Cell migration</subject><subject>Cell Proliferation</subject><subject>Cell self-renewal</subject><subject>CRISPR</subject><subject>Female</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Gli1 protein</subject><subject>Glioblastoma</subject><subject>Glioma - genetics</subject><subject>Glioma - metabolism</subject><subject>Glioma - pathology</subject><subject>Glioma cells</subject><subject>Hedgehog protein</subject><subject>Hedgehog Proteins - metabolism</subject><subject>Humans</subject><subject>Immunoprecipitation</subject><subject>Invasiveness</subject><subject>Male</subject><subject>Mice, Inbred BALB C</subject><subject>Mice, Nude</subject><subject>Middle Aged</subject><subject>Models, Biological</subject><subject>mRNA</subject><subject>Neoplasm Invasiveness</subject><subject>Neoplastic Stem Cells - metabolism</subject><subject>Neoplastic Stem Cells - pathology</subject><subject>Oncology</subject><subject>Original Paper</subject><subject>Pathology</subject><subject>Phenotype</subject><subject>Phosphorylation</subject><subject>RNA, Messenger - genetics</subject><subject>RNA, Messenger - metabolism</subject><subject>RNA-Binding Proteins - genetics</subject><subject>RNA-Binding Proteins - metabolism</subject><subject>Signal Transduction</subject><subject>Stem cell transplantation</subject><subject>Stem cells</subject><subject>Survival Analysis</subject><subject>Xenografts</subject><subject>Zinc Finger Protein GLI1 - metabolism</subject><subject>Zinc finger proteins</subject><issn>2211-3428</issn><issn>2211-3436</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kU1LAzEQhoMoKuof8CABL17W5mOT3T1K0bZYEFHPIZtMamQ_6mar7b83tbWCBwkhQ-aZd4Z5ETqn5JoSkg0C5SlhCaFFQkgqebLcQ8eMUZrwlMv9XczyI3QWwhsha4xKIQ_REaesiIccI_V4P8EWnDceGrPCtfZNH2_As8q3tcahhxobqKrvqIEQcLnC2vT-Q_e-meH-FfDTeDwYTScUBz9rdLX-nuv-9VOvTtGB01WAs-17gl7ubp-H42T6MJoMb6aJ4ZnoE5uZUhScGZu5VBijwUFKizLnpSPWZVbkwuYOsjy1pbbWgYx5WUBGhKM04yfoaqM779r3BYRe1T6sx9YNtIugGBOSEiFTGtHLP-hbu-ji2JHiVMblEiIixTaU6doQOnBq3vladytFiVo7oDYOqOiA-nZALWPRxVZ6UdZgdyU_-44A3wAhppoZdL-9_5H9AoWKkWU</recordid><startdate>20191201</startdate><enddate>20191201</enddate><creator>Han, Bo</creator><creator>Wang, Ruijia</creator><creator>Chen, Yongjie</creator><creator>Meng, Xiangqi</creator><creator>Wu, Pengfei</creator><creator>Li, Ziwei</creator><creator>Duan, Chunbin</creator><creator>Li, Qingbin</creator><creator>Li, Yang</creator><creator>Zhao, Shihong</creator><creator>Jiang, Chuanlu</creator><creator>Cai, Jinquan</creator><general>Springer Netherlands</general><general>Springer Nature B.V</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></search><sort><creationdate>20191201</creationdate><title>QKI deficiency maintains glioma stem cell stemness by activating the SHH/GLI1 signaling pathway</title><author>Han, Bo ; Wang, Ruijia ; Chen, Yongjie ; Meng, Xiangqi ; Wu, Pengfei ; Li, Ziwei ; Duan, Chunbin ; Li, Qingbin ; Li, Yang ; Zhao, Shihong ; Jiang, Chuanlu ; Cai, Jinquan</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c375t-d7cb5932cd7f45ccaefe419b83bf0df7d585d8fe784dbaddfe6e4169e705f1173</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Aged</topic><topic>Animals</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Brain Neoplasms - genetics</topic><topic>Brain Neoplasms - metabolism</topic><topic>Brain Neoplasms - pathology</topic><topic>Cancer Research</topic><topic>Cell Line, Tumor</topic><topic>Cell migration</topic><topic>Cell Proliferation</topic><topic>Cell self-renewal</topic><topic>CRISPR</topic><topic>Female</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Gli1 protein</topic><topic>Glioblastoma</topic><topic>Glioma - genetics</topic><topic>Glioma - metabolism</topic><topic>Glioma - pathology</topic><topic>Glioma cells</topic><topic>Hedgehog protein</topic><topic>Hedgehog Proteins - metabolism</topic><topic>Humans</topic><topic>Immunoprecipitation</topic><topic>Invasiveness</topic><topic>Male</topic><topic>Mice, Inbred BALB C</topic><topic>Mice, Nude</topic><topic>Middle Aged</topic><topic>Models, Biological</topic><topic>mRNA</topic><topic>Neoplasm Invasiveness</topic><topic>Neoplastic Stem Cells - metabolism</topic><topic>Neoplastic Stem Cells - pathology</topic><topic>Oncology</topic><topic>Original Paper</topic><topic>Pathology</topic><topic>Phenotype</topic><topic>Phosphorylation</topic><topic>RNA, Messenger - genetics</topic><topic>RNA, Messenger - metabolism</topic><topic>RNA-Binding Proteins - genetics</topic><topic>RNA-Binding Proteins - metabolism</topic><topic>Signal Transduction</topic><topic>Stem cell transplantation</topic><topic>Stem cells</topic><topic>Survival Analysis</topic><topic>Xenografts</topic><topic>Zinc Finger Protein GLI1 - metabolism</topic><topic>Zinc finger proteins</topic><toplevel>online_resources</toplevel><creatorcontrib>Han, Bo</creatorcontrib><creatorcontrib>Wang, Ruijia</creatorcontrib><creatorcontrib>Chen, Yongjie</creatorcontrib><creatorcontrib>Meng, Xiangqi</creatorcontrib><creatorcontrib>Wu, Pengfei</creatorcontrib><creatorcontrib>Li, Ziwei</creatorcontrib><creatorcontrib>Duan, Chunbin</creatorcontrib><creatorcontrib>Li, Qingbin</creatorcontrib><creatorcontrib>Li, Yang</creatorcontrib><creatorcontrib>Zhao, Shihong</creatorcontrib><creatorcontrib>Jiang, Chuanlu</creatorcontrib><creatorcontrib>Cai, Jinquan</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><jtitle>Cellular oncology (Dordrecht)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Han, Bo</au><au>Wang, Ruijia</au><au>Chen, Yongjie</au><au>Meng, Xiangqi</au><au>Wu, Pengfei</au><au>Li, Ziwei</au><au>Duan, Chunbin</au><au>Li, Qingbin</au><au>Li, Yang</au><au>Zhao, Shihong</au><au>Jiang, Chuanlu</au><au>Cai, Jinquan</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>QKI deficiency maintains glioma stem cell stemness by activating the SHH/GLI1 signaling pathway</atitle><jtitle>Cellular oncology (Dordrecht)</jtitle><stitle>Cell Oncol</stitle><addtitle>Cell Oncol (Dordr)</addtitle><date>2019-12-01</date><risdate>2019</risdate><volume>42</volume><issue>6</issue><spage>801</spage><epage>813</epage><pages>801-813</pages><issn>2211-3428</issn><eissn>2211-3436</eissn><abstract>Purpose
Glioblastoma (GBM) stem cells (GSCs) have been found to be the main cause of malignant GBM progression. It has also been found that Quaking homolog (QKI
)
plays a predominant role in driving GBM development. Here, we aimed to asses the role of QKI in maintaining GSC stemness and inducing the invasiveness of GBM cells.
Methods
Public databases were used to assess the expression of QKI and its correlation with stemness markers in primary GBMs. The CRISPR-Cas9 technology was used to generate
QK
I knockout GBM cells, and RNA immunoprecipitation was used to assess QKI-
GLI1
protein-mRNA interactions. In addition, in vitro and in vivo GBM cell proliferation, migration, xenografting and neurosphere formation assays were performed.
Results
Using public GBM databases, QKI was identified as a potential GSC regulator. We found that QKI could inhibit stem-like cell (SLC) stemness and prolong the survival of xenografted mice. Mechanistically, we found that
QKI
knockout increased the GLI Family Zinc Finger 1 (
GLI1
) mRNA level, which is essential for maintaining the self-renewal ability of GSCs. In addition, we found that
QKI
knockout activated the Hedgehog signaling pathway via Tra-2 and GLI response element (TGE)-specific
GLI1
mRNA disruption.
Conclusion
Our data indicate that upregulation of GLI1 induced by QKI deficiency maintains GSC stemness and enhances the invasiveness of GBM cells, thereby hinting at new options for the treatment of GBM.</abstract><cop>Dordrecht</cop><pub>Springer Netherlands</pub><pmid>31292920</pmid><doi>10.1007/s13402-019-00463-x</doi><tpages>13</tpages></addata></record> |
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| subjects | Aged Animals Biomedical and Life Sciences Biomedicine Brain Neoplasms - genetics Brain Neoplasms - metabolism Brain Neoplasms - pathology Cancer Research Cell Line, Tumor Cell migration Cell Proliferation Cell self-renewal CRISPR Female Gene Expression Regulation, Neoplastic Gli1 protein Glioblastoma Glioma - genetics Glioma - metabolism Glioma - pathology Glioma cells Hedgehog protein Hedgehog Proteins - metabolism Humans Immunoprecipitation Invasiveness Male Mice, Inbred BALB C Mice, Nude Middle Aged Models, Biological mRNA Neoplasm Invasiveness Neoplastic Stem Cells - metabolism Neoplastic Stem Cells - pathology Oncology Original Paper Pathology Phenotype Phosphorylation RNA, Messenger - genetics RNA, Messenger - metabolism RNA-Binding Proteins - genetics RNA-Binding Proteins - metabolism Signal Transduction Stem cell transplantation Stem cells Survival Analysis Xenografts Zinc Finger Protein GLI1 - metabolism Zinc finger proteins |
| title | QKI deficiency maintains glioma stem cell stemness by activating the SHH/GLI1 signaling pathway |
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