Long noncoding RNA SNHG9 facilitates growth of glioma stem‐like cells via miR‐326/SOX9 axis

Background Glioma stem‐like cells (GSCs) are greatly responsible for the progression of glioma. Long noncoding RNAs (lncRNAs) play an important role in glioma tumor progression. This study aims to explore the role and underlying mechanism of lncRNA SNHG9 in regulating GSC cell growth. Methods GSCs w...

Ausführliche Beschreibung

Gespeichert in:
Bibliographische Detailangaben
Veröffentlicht in:The journal of gene medicine 2022-01, Vol.24 (1), p.e3334-n/a
Hauptverfasser: Wang, Chao‐Jie, Chao, Chu‐Rui, Zhao, Wei‐Feng, Liu, Hui‐Min, Feng, Jiang‐Shan, Cui, Yong‐Xia
Format: Artikel
Sprache:eng
Schlagworte:
Online-Zugang:Volltext
Tags: Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
container_end_page n/a
container_issue 1
container_start_page e3334
container_title The journal of gene medicine
container_volume 24
creator Wang, Chao‐Jie
Chao, Chu‐Rui
Zhao, Wei‐Feng
Liu, Hui‐Min
Feng, Jiang‐Shan
Cui, Yong‐Xia
description Background Glioma stem‐like cells (GSCs) are greatly responsible for the progression of glioma. Long noncoding RNAs (lncRNAs) play an important role in glioma tumor progression. This study aims to explore the role and underlying mechanism of lncRNA SNHG9 in regulating GSC cell growth. Methods GSCs were obtained from glioma cells (U87 and U251) and referred to as GSC‐87 and GSC‐251, respectively. The interactions between miR‐326 and SNHG9 or SOX9 were analyzed using luciferase reporter assay. Cell growth of GSCs was evaluated by EdU assay and sphere formation assay. Results SNHG9 expression was significantly higher in GSC‐87 and GSC‐251 cells than in U87 and U251 cells. SNHG9 overexpression promoted GSC cell growth, whereas SNHG9 knockdown inhibited GSC cell growth. Mechanistically, SNHG9 acted as a competitive endogenous RNA of miR‐326 to elevate the expression of SOX9, a direct target of miR‐326. Moreover, transfection with miR‐326 inhibitor counteracted SNHG9 knockdown‐mediated inhibition of GSC cell growth. Conclusions SNHG9 facilitates growth of GSCs via the miR‐326/SOX9 axis. This study provides a promising therapeutic target for glioma treatment. LncRNA SNHG9 functions as a ceRNA of miR‐326 to elevate expression of SOX9, and thereby promotes cell proliferation of glioma stem cells (GSCs). Our findings suggest that SNHG9 may be a promising therapeutic target for the treatment of glioma.
doi_str_mv 10.1002/jgm.3334
format Article
fullrecord <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_2507730334</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2615878287</sourcerecordid><originalsourceid>FETCH-LOGICAL-c3494-a738a96b68d9bb0e7f945a08eb7efbb70becb95395228856b48f9eeb4b5331ae3</originalsourceid><addsrcrecordid>eNp1kM1KAzEUhYMo_lTBJ5CAGzfTZpLJJFmKaFWqharQXUimd2rqzEQnU6s7H8Fn9EkcrT8guLqHy8fH4SC0G5NuTAjtzaZllzGWrKDNmNM4opQnq20mSkWJkuMNtBXCjJBYSKnW0QZjQirG1SbSA19NceWrzE9cm0aXh_jq8rSvcG4yV7jGNBDwtPaL5hb7HE8L50uDQwPl28tr4e4AZ1AUAT86g0s3ap-Mpr2r4Vhh8-TCNlrLTRFg5-t20M3J8fXRaTQY9s-ODgdRxhKVREYwaVRqUzlR1hIQuUq4IRKsgNxaQSxkVnGmOKVS8tQmMlcANrGcsdgA66CDpfe-9g9zCI0uXfhoZirw86ApJ0Iw0m7Uovt_0Jmf11XbTtM05lJIKsWvMKt9CDXk-r52pamfdUz0x-i6HV2zpXDvSzi3JUx-wO-VWyBaAgtXwPO_In3ev_gUvgM6Yoq9</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2615878287</pqid></control><display><type>article</type><title>Long noncoding RNA SNHG9 facilitates growth of glioma stem‐like cells via miR‐326/SOX9 axis</title><source>MEDLINE</source><source>Wiley Journals</source><creator>Wang, Chao‐Jie ; Chao, Chu‐Rui ; Zhao, Wei‐Feng ; Liu, Hui‐Min ; Feng, Jiang‐Shan ; Cui, Yong‐Xia</creator><creatorcontrib>Wang, Chao‐Jie ; Chao, Chu‐Rui ; Zhao, Wei‐Feng ; Liu, Hui‐Min ; Feng, Jiang‐Shan ; Cui, Yong‐Xia</creatorcontrib><description>Background Glioma stem‐like cells (GSCs) are greatly responsible for the progression of glioma. Long noncoding RNAs (lncRNAs) play an important role in glioma tumor progression. This study aims to explore the role and underlying mechanism of lncRNA SNHG9 in regulating GSC cell growth. Methods GSCs were obtained from glioma cells (U87 and U251) and referred to as GSC‐87 and GSC‐251, respectively. The interactions between miR‐326 and SNHG9 or SOX9 were analyzed using luciferase reporter assay. Cell growth of GSCs was evaluated by EdU assay and sphere formation assay. Results SNHG9 expression was significantly higher in GSC‐87 and GSC‐251 cells than in U87 and U251 cells. SNHG9 overexpression promoted GSC cell growth, whereas SNHG9 knockdown inhibited GSC cell growth. Mechanistically, SNHG9 acted as a competitive endogenous RNA of miR‐326 to elevate the expression of SOX9, a direct target of miR‐326. Moreover, transfection with miR‐326 inhibitor counteracted SNHG9 knockdown‐mediated inhibition of GSC cell growth. Conclusions SNHG9 facilitates growth of GSCs via the miR‐326/SOX9 axis. This study provides a promising therapeutic target for glioma treatment. LncRNA SNHG9 functions as a ceRNA of miR‐326 to elevate expression of SOX9, and thereby promotes cell proliferation of glioma stem cells (GSCs). Our findings suggest that SNHG9 may be a promising therapeutic target for the treatment of glioma.</description><identifier>ISSN: 1099-498X</identifier><identifier>EISSN: 1521-2254</identifier><identifier>DOI: 10.1002/jgm.3334</identifier><identifier>PMID: 33789359</identifier><language>eng</language><publisher>England: Wiley Periodicals Inc</publisher><subject>Brain Neoplasms - genetics ; Brain Neoplasms - pathology ; Brain tumors ; Cell growth ; Cell Line, Tumor ; Cell Proliferation - genetics ; Gene Expression Regulation, Neoplastic ; Gene therapy ; Glioma ; Glioma - pathology ; Glioma cells ; glioma stem cell ; Humans ; MicroRNAs - genetics ; MicroRNAs - metabolism ; miR‐326 ; Neoplastic Stem Cells - metabolism ; Neoplastic Stem Cells - pathology ; Non-coding RNA ; RNA, Long Noncoding - genetics ; RNA, Long Noncoding - metabolism ; SNHG9 ; SOX9 ; Sox9 protein ; SOX9 Transcription Factor - genetics ; SOX9 Transcription Factor - metabolism ; Therapeutic targets ; Transfection</subject><ispartof>The journal of gene medicine, 2022-01, Vol.24 (1), p.e3334-n/a</ispartof><rights>2021 John Wiley &amp; Sons, Ltd.</rights><rights>2022 John Wiley &amp; Sons, Ltd.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3494-a738a96b68d9bb0e7f945a08eb7efbb70becb95395228856b48f9eeb4b5331ae3</citedby><cites>FETCH-LOGICAL-c3494-a738a96b68d9bb0e7f945a08eb7efbb70becb95395228856b48f9eeb4b5331ae3</cites><orcidid>0000-0001-7887-315X</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fjgm.3334$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fjgm.3334$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,780,784,1417,27924,27925,45574,45575</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/33789359$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wang, Chao‐Jie</creatorcontrib><creatorcontrib>Chao, Chu‐Rui</creatorcontrib><creatorcontrib>Zhao, Wei‐Feng</creatorcontrib><creatorcontrib>Liu, Hui‐Min</creatorcontrib><creatorcontrib>Feng, Jiang‐Shan</creatorcontrib><creatorcontrib>Cui, Yong‐Xia</creatorcontrib><title>Long noncoding RNA SNHG9 facilitates growth of glioma stem‐like cells via miR‐326/SOX9 axis</title><title>The journal of gene medicine</title><addtitle>J Gene Med</addtitle><description>Background Glioma stem‐like cells (GSCs) are greatly responsible for the progression of glioma. Long noncoding RNAs (lncRNAs) play an important role in glioma tumor progression. This study aims to explore the role and underlying mechanism of lncRNA SNHG9 in regulating GSC cell growth. Methods GSCs were obtained from glioma cells (U87 and U251) and referred to as GSC‐87 and GSC‐251, respectively. The interactions between miR‐326 and SNHG9 or SOX9 were analyzed using luciferase reporter assay. Cell growth of GSCs was evaluated by EdU assay and sphere formation assay. Results SNHG9 expression was significantly higher in GSC‐87 and GSC‐251 cells than in U87 and U251 cells. SNHG9 overexpression promoted GSC cell growth, whereas SNHG9 knockdown inhibited GSC cell growth. Mechanistically, SNHG9 acted as a competitive endogenous RNA of miR‐326 to elevate the expression of SOX9, a direct target of miR‐326. Moreover, transfection with miR‐326 inhibitor counteracted SNHG9 knockdown‐mediated inhibition of GSC cell growth. Conclusions SNHG9 facilitates growth of GSCs via the miR‐326/SOX9 axis. This study provides a promising therapeutic target for glioma treatment. LncRNA SNHG9 functions as a ceRNA of miR‐326 to elevate expression of SOX9, and thereby promotes cell proliferation of glioma stem cells (GSCs). Our findings suggest that SNHG9 may be a promising therapeutic target for the treatment of glioma.</description><subject>Brain Neoplasms - genetics</subject><subject>Brain Neoplasms - pathology</subject><subject>Brain tumors</subject><subject>Cell growth</subject><subject>Cell Line, Tumor</subject><subject>Cell Proliferation - genetics</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Gene therapy</subject><subject>Glioma</subject><subject>Glioma - pathology</subject><subject>Glioma cells</subject><subject>glioma stem cell</subject><subject>Humans</subject><subject>MicroRNAs - genetics</subject><subject>MicroRNAs - metabolism</subject><subject>miR‐326</subject><subject>Neoplastic Stem Cells - metabolism</subject><subject>Neoplastic Stem Cells - pathology</subject><subject>Non-coding RNA</subject><subject>RNA, Long Noncoding - genetics</subject><subject>RNA, Long Noncoding - metabolism</subject><subject>SNHG9</subject><subject>SOX9</subject><subject>Sox9 protein</subject><subject>SOX9 Transcription Factor - genetics</subject><subject>SOX9 Transcription Factor - metabolism</subject><subject>Therapeutic targets</subject><subject>Transfection</subject><issn>1099-498X</issn><issn>1521-2254</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kM1KAzEUhYMo_lTBJ5CAGzfTZpLJJFmKaFWqharQXUimd2rqzEQnU6s7H8Fn9EkcrT8guLqHy8fH4SC0G5NuTAjtzaZllzGWrKDNmNM4opQnq20mSkWJkuMNtBXCjJBYSKnW0QZjQirG1SbSA19NceWrzE9cm0aXh_jq8rSvcG4yV7jGNBDwtPaL5hb7HE8L50uDQwPl28tr4e4AZ1AUAT86g0s3ap-Mpr2r4Vhh8-TCNlrLTRFg5-t20M3J8fXRaTQY9s-ODgdRxhKVREYwaVRqUzlR1hIQuUq4IRKsgNxaQSxkVnGmOKVS8tQmMlcANrGcsdgA66CDpfe-9g9zCI0uXfhoZirw86ApJ0Iw0m7Uovt_0Jmf11XbTtM05lJIKsWvMKt9CDXk-r52pamfdUz0x-i6HV2zpXDvSzi3JUx-wO-VWyBaAgtXwPO_In3ev_gUvgM6Yoq9</recordid><startdate>202201</startdate><enddate>202201</enddate><creator>Wang, Chao‐Jie</creator><creator>Chao, Chu‐Rui</creator><creator>Zhao, Wei‐Feng</creator><creator>Liu, Hui‐Min</creator><creator>Feng, Jiang‐Shan</creator><creator>Cui, Yong‐Xia</creator><general>Wiley Periodicals Inc</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>7QP</scope><scope>7TK</scope><scope>7TM</scope><scope>8FD</scope><scope>FR3</scope><scope>K9.</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0001-7887-315X</orcidid></search><sort><creationdate>202201</creationdate><title>Long noncoding RNA SNHG9 facilitates growth of glioma stem‐like cells via miR‐326/SOX9 axis</title><author>Wang, Chao‐Jie ; Chao, Chu‐Rui ; Zhao, Wei‐Feng ; Liu, Hui‐Min ; Feng, Jiang‐Shan ; Cui, Yong‐Xia</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3494-a738a96b68d9bb0e7f945a08eb7efbb70becb95395228856b48f9eeb4b5331ae3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>Brain Neoplasms - genetics</topic><topic>Brain Neoplasms - pathology</topic><topic>Brain tumors</topic><topic>Cell growth</topic><topic>Cell Line, Tumor</topic><topic>Cell Proliferation - genetics</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Gene therapy</topic><topic>Glioma</topic><topic>Glioma - pathology</topic><topic>Glioma cells</topic><topic>glioma stem cell</topic><topic>Humans</topic><topic>MicroRNAs - genetics</topic><topic>MicroRNAs - metabolism</topic><topic>miR‐326</topic><topic>Neoplastic Stem Cells - metabolism</topic><topic>Neoplastic Stem Cells - pathology</topic><topic>Non-coding RNA</topic><topic>RNA, Long Noncoding - genetics</topic><topic>RNA, Long Noncoding - metabolism</topic><topic>SNHG9</topic><topic>SOX9</topic><topic>Sox9 protein</topic><topic>SOX9 Transcription Factor - genetics</topic><topic>SOX9 Transcription Factor - metabolism</topic><topic>Therapeutic targets</topic><topic>Transfection</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wang, Chao‐Jie</creatorcontrib><creatorcontrib>Chao, Chu‐Rui</creatorcontrib><creatorcontrib>Zhao, Wei‐Feng</creatorcontrib><creatorcontrib>Liu, Hui‐Min</creatorcontrib><creatorcontrib>Feng, Jiang‐Shan</creatorcontrib><creatorcontrib>Cui, Yong‐Xia</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Calcium &amp; Calcified Tissue Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>ProQuest Health &amp; Medical Complete (Alumni)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>The journal of gene medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wang, Chao‐Jie</au><au>Chao, Chu‐Rui</au><au>Zhao, Wei‐Feng</au><au>Liu, Hui‐Min</au><au>Feng, Jiang‐Shan</au><au>Cui, Yong‐Xia</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Long noncoding RNA SNHG9 facilitates growth of glioma stem‐like cells via miR‐326/SOX9 axis</atitle><jtitle>The journal of gene medicine</jtitle><addtitle>J Gene Med</addtitle><date>2022-01</date><risdate>2022</risdate><volume>24</volume><issue>1</issue><spage>e3334</spage><epage>n/a</epage><pages>e3334-n/a</pages><issn>1099-498X</issn><eissn>1521-2254</eissn><abstract>Background Glioma stem‐like cells (GSCs) are greatly responsible for the progression of glioma. Long noncoding RNAs (lncRNAs) play an important role in glioma tumor progression. This study aims to explore the role and underlying mechanism of lncRNA SNHG9 in regulating GSC cell growth. Methods GSCs were obtained from glioma cells (U87 and U251) and referred to as GSC‐87 and GSC‐251, respectively. The interactions between miR‐326 and SNHG9 or SOX9 were analyzed using luciferase reporter assay. Cell growth of GSCs was evaluated by EdU assay and sphere formation assay. Results SNHG9 expression was significantly higher in GSC‐87 and GSC‐251 cells than in U87 and U251 cells. SNHG9 overexpression promoted GSC cell growth, whereas SNHG9 knockdown inhibited GSC cell growth. Mechanistically, SNHG9 acted as a competitive endogenous RNA of miR‐326 to elevate the expression of SOX9, a direct target of miR‐326. Moreover, transfection with miR‐326 inhibitor counteracted SNHG9 knockdown‐mediated inhibition of GSC cell growth. Conclusions SNHG9 facilitates growth of GSCs via the miR‐326/SOX9 axis. This study provides a promising therapeutic target for glioma treatment. LncRNA SNHG9 functions as a ceRNA of miR‐326 to elevate expression of SOX9, and thereby promotes cell proliferation of glioma stem cells (GSCs). Our findings suggest that SNHG9 may be a promising therapeutic target for the treatment of glioma.</abstract><cop>England</cop><pub>Wiley Periodicals Inc</pub><pmid>33789359</pmid><doi>10.1002/jgm.3334</doi><tpages>10</tpages><orcidid>https://orcid.org/0000-0001-7887-315X</orcidid></addata></record>
fulltext fulltext
identifier ISSN: 1099-498X
ispartof The journal of gene medicine, 2022-01, Vol.24 (1), p.e3334-n/a
issn 1099-498X
1521-2254
language eng
recordid cdi_proquest_miscellaneous_2507730334
source MEDLINE; Wiley Journals
subjects Brain Neoplasms - genetics
Brain Neoplasms - pathology
Brain tumors
Cell growth
Cell Line, Tumor
Cell Proliferation - genetics
Gene Expression Regulation, Neoplastic
Gene therapy
Glioma
Glioma - pathology
Glioma cells
glioma stem cell
Humans
MicroRNAs - genetics
MicroRNAs - metabolism
miR‐326
Neoplastic Stem Cells - metabolism
Neoplastic Stem Cells - pathology
Non-coding RNA
RNA, Long Noncoding - genetics
RNA, Long Noncoding - metabolism
SNHG9
SOX9
Sox9 protein
SOX9 Transcription Factor - genetics
SOX9 Transcription Factor - metabolism
Therapeutic targets
Transfection
title Long noncoding RNA SNHG9 facilitates growth of glioma stem‐like cells via miR‐326/SOX9 axis
url https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-04T12%3A08%3A52IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Long%20noncoding%20RNA%20SNHG9%20facilitates%20growth%20of%20glioma%20stem%E2%80%90like%20cells%20via%20miR%E2%80%90326/SOX9%20axis&rft.jtitle=The%20journal%20of%20gene%20medicine&rft.au=Wang,%20Chao%E2%80%90Jie&rft.date=2022-01&rft.volume=24&rft.issue=1&rft.spage=e3334&rft.epage=n/a&rft.pages=e3334-n/a&rft.issn=1099-498X&rft.eissn=1521-2254&rft_id=info:doi/10.1002/jgm.3334&rft_dat=%3Cproquest_cross%3E2615878287%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2615878287&rft_id=info:pmid/33789359&rfr_iscdi=true