HOXC6 Regulates the Epithelial-Mesenchymal Transition through the TGF-β/Smad Signaling Pathway and Predicts a Poor Prognosis in Glioblastoma
Background. The HOX gene family of transcription factors, characterized by conserved homeodomains, is positively correlated with the resistance to chemotherapy drugs and poor prognosis, as well as the initiating potential of gliomas. However, there are few studies regarding the HOXC6 gene in glioma...
Gespeichert in:
| Veröffentlicht in: | Journal of oncology 2022-05, Vol.2022, p.8016102-18 |
|---|---|
| Hauptverfasser: | , , , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 18 |
|---|---|
| container_issue | |
| container_start_page | 8016102 |
| container_title | Journal of oncology |
| container_volume | 2022 |
| creator | Eryi, Sun Zheng, Li Honghua, Cai Su, Zhao Han, Xie Donggang, Pan Zhou, Zhou Liping, Zhan Bo, Chen |
| description | Background. The HOX gene family of transcription factors, characterized by conserved homeodomains, is positively correlated with the resistance to chemotherapy drugs and poor prognosis, as well as the initiating potential of gliomas. However, there are few studies regarding the HOXC6 gene in glioma cells. Therefore, in the present study, we explored the regulatory roles and detailed mechanisms underlying the relationship between HOXC6 and the progression of GBM. Methods. The expression levels and prognostic value of HOXC6 in GBM were evaluated using the data obtained from the GCCA, GEPIA, and ONCOMINE databases. The relationship between GBM prognosis and levels of HOXC6 was identified using Kaplan-Meier curves. The protein levels of HOXC6 in GBM and adjacent normal tissues were identified via Western blot and immunohistochemistry (IHC) staining methods. Lentiviruses containing full-length HOXC6 and HOXC6 specific siRNA sequences were used to overexpress and knock down, respectively, the expression of HOXC6 in U87 and U251 cells. The role of HOXC6 in the regulation of migration and proliferation of GBM cells was accessed using Transwell, wound healing, CCK-8, and colony formation assays. The activation of the TGF-β/Smad signaling pathway was detected via Western blotting. Results. Compared to normal tissues and control cells, GBM tissues and cell lines showed higher expressions of HOXC6. The expression of HOXC6 was associated with disease-free and the overall survival of GBM patients. Additionally, positive correlations between the expression of HOXC6 and the migration and proliferation of GBM cells were observed in vitro. The mechanistic analyses indicated that HOXC6 exerts its promotive effect on the progression and invasion of glioma cells by promoting the activation of the EMT and TGF-β/Smad signaling pathways. Conclusions. HOXC6 enhances the migration and proliferation of GBM by activating the EMT signaling pathway. |
| doi_str_mv | 10.1155/2022/8016102 |
| format | Article |
| fullrecord | <record><control><sourceid>gale_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_9098331</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><galeid>A703852543</galeid><sourcerecordid>A703852543</sourcerecordid><originalsourceid>FETCH-LOGICAL-c476t-3e6a9aad534cc903d28a1d5c4e13dc81bcfb72cf4c70a1960b9b5c90791e46953</originalsourceid><addsrcrecordid>eNp90s9u0zAcB_AIgdgY3DgjS1yQINRObCe5IE3V1iENrWJF4mb94jiJJ8cudsLUh9jL7EF4Jty1TIUDp58tf_T1v1-SvCb4IyGMzTKcZbMSE05w9iQ5Jrws0pIy_PRgfJS8COEGY05xxZ8nRzljBaEVOU7uLq6-zzn6qrrJwKgCGnuFztY6FqPBpF9UUFb2mwEMWnmwQY_a2ai8m7r-Qa8W5-mv-9n1AA261p0Fo22HljD2t7BBYBu09KrRcgwI0NI5H-eusy7ogLRFC6NdbSCMboCXybMWTFCv9vUk-XZ-tppfpJdXi8_z08tU0oKPaa44VAANy6mUFc6brATSMEkVyRtZklq2dZHJlsoCA6k4rquaRVhURFFesfwk-bTLXU_1oBqp7OjBiLXXA_iNcKDF3ytW96JzP0WFqzLPSQx4tw_w7sekwigGHaQyBqxyUxAZ54xgmhVFpG__oTdu8vGVHhTlpMT0QHVglNC2dXFfuQ0VpwXOS5Yxmkf1YaekdyF41T4emWCx7Qax7Qax74bI3xxe8xH_-f4I3u9Ar20Dt_r_cb8BI6e9lA</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2664618047</pqid></control><display><type>article</type><title>HOXC6 Regulates the Epithelial-Mesenchymal Transition through the TGF-β/Smad Signaling Pathway and Predicts a Poor Prognosis in Glioblastoma</title><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>PubMed Central Open Access</source><source>Wiley Online Library Open Access</source><source>PubMed Central</source><source>Alma/SFX Local Collection</source><creator>Eryi, Sun ; Zheng, Li ; Honghua, Cai ; Su, Zhao ; Han, Xie ; Donggang, Pan ; Zhou, Zhou ; Liping, Zhan ; Bo, Chen</creator><contributor>Wang, Jimei ; Jimei Wang</contributor><creatorcontrib>Eryi, Sun ; Zheng, Li ; Honghua, Cai ; Su, Zhao ; Han, Xie ; Donggang, Pan ; Zhou, Zhou ; Liping, Zhan ; Bo, Chen ; Wang, Jimei ; Jimei Wang</creatorcontrib><description>Background. The HOX gene family of transcription factors, characterized by conserved homeodomains, is positively correlated with the resistance to chemotherapy drugs and poor prognosis, as well as the initiating potential of gliomas. However, there are few studies regarding the HOXC6 gene in glioma cells. Therefore, in the present study, we explored the regulatory roles and detailed mechanisms underlying the relationship between HOXC6 and the progression of GBM. Methods. The expression levels and prognostic value of HOXC6 in GBM were evaluated using the data obtained from the GCCA, GEPIA, and ONCOMINE databases. The relationship between GBM prognosis and levels of HOXC6 was identified using Kaplan-Meier curves. The protein levels of HOXC6 in GBM and adjacent normal tissues were identified via Western blot and immunohistochemistry (IHC) staining methods. Lentiviruses containing full-length HOXC6 and HOXC6 specific siRNA sequences were used to overexpress and knock down, respectively, the expression of HOXC6 in U87 and U251 cells. The role of HOXC6 in the regulation of migration and proliferation of GBM cells was accessed using Transwell, wound healing, CCK-8, and colony formation assays. The activation of the TGF-β/Smad signaling pathway was detected via Western blotting. Results. Compared to normal tissues and control cells, GBM tissues and cell lines showed higher expressions of HOXC6. The expression of HOXC6 was associated with disease-free and the overall survival of GBM patients. Additionally, positive correlations between the expression of HOXC6 and the migration and proliferation of GBM cells were observed in vitro. The mechanistic analyses indicated that HOXC6 exerts its promotive effect on the progression and invasion of glioma cells by promoting the activation of the EMT and TGF-β/Smad signaling pathways. Conclusions. HOXC6 enhances the migration and proliferation of GBM by activating the EMT signaling pathway.</description><identifier>ISSN: 1687-8450</identifier><identifier>EISSN: 1687-8450</identifier><identifier>DOI: 10.1155/2022/8016102</identifier><identifier>PMID: 35571491</identifier><language>eng</language><publisher>Egypt: Hindawi</publisher><subject>Analysis ; Apoptosis ; Blood diseases ; Brain cancer ; Cancer ; Chemotherapy ; Gene expression ; Genes ; Genetic aspects ; Genetic transcription ; Gliomas ; Growth factors ; Immunohistochemistry ; Medical prognosis ; Metastasis ; Nervous system ; Prognosis ; Radiation therapy ; Stem cells ; Transcription factors ; Transforming growth factors ; Tumors ; Wound healing</subject><ispartof>Journal of oncology, 2022-05, Vol.2022, p.8016102-18</ispartof><rights>Copyright © 2022 Sun Eryi et al.</rights><rights>COPYRIGHT 2022 John Wiley & Sons, Inc.</rights><rights>Copyright © 2022 Sun Eryi et al. This work is licensed 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><rights>Copyright © 2022 Sun Eryi et al. 2022</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c476t-3e6a9aad534cc903d28a1d5c4e13dc81bcfb72cf4c70a1960b9b5c90791e46953</citedby><cites>FETCH-LOGICAL-c476t-3e6a9aad534cc903d28a1d5c4e13dc81bcfb72cf4c70a1960b9b5c90791e46953</cites><orcidid>0000-0003-1756-5000 ; 0000-0002-6772-1246</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/PMC9098331/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC9098331/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,724,777,781,882,27905,27906,53772,53774</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/35571491$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Wang, Jimei</contributor><contributor>Jimei Wang</contributor><creatorcontrib>Eryi, Sun</creatorcontrib><creatorcontrib>Zheng, Li</creatorcontrib><creatorcontrib>Honghua, Cai</creatorcontrib><creatorcontrib>Su, Zhao</creatorcontrib><creatorcontrib>Han, Xie</creatorcontrib><creatorcontrib>Donggang, Pan</creatorcontrib><creatorcontrib>Zhou, Zhou</creatorcontrib><creatorcontrib>Liping, Zhan</creatorcontrib><creatorcontrib>Bo, Chen</creatorcontrib><title>HOXC6 Regulates the Epithelial-Mesenchymal Transition through the TGF-β/Smad Signaling Pathway and Predicts a Poor Prognosis in Glioblastoma</title><title>Journal of oncology</title><addtitle>J Oncol</addtitle><description>Background. The HOX gene family of transcription factors, characterized by conserved homeodomains, is positively correlated with the resistance to chemotherapy drugs and poor prognosis, as well as the initiating potential of gliomas. However, there are few studies regarding the HOXC6 gene in glioma cells. Therefore, in the present study, we explored the regulatory roles and detailed mechanisms underlying the relationship between HOXC6 and the progression of GBM. Methods. The expression levels and prognostic value of HOXC6 in GBM were evaluated using the data obtained from the GCCA, GEPIA, and ONCOMINE databases. The relationship between GBM prognosis and levels of HOXC6 was identified using Kaplan-Meier curves. The protein levels of HOXC6 in GBM and adjacent normal tissues were identified via Western blot and immunohistochemistry (IHC) staining methods. Lentiviruses containing full-length HOXC6 and HOXC6 specific siRNA sequences were used to overexpress and knock down, respectively, the expression of HOXC6 in U87 and U251 cells. The role of HOXC6 in the regulation of migration and proliferation of GBM cells was accessed using Transwell, wound healing, CCK-8, and colony formation assays. The activation of the TGF-β/Smad signaling pathway was detected via Western blotting. Results. Compared to normal tissues and control cells, GBM tissues and cell lines showed higher expressions of HOXC6. The expression of HOXC6 was associated with disease-free and the overall survival of GBM patients. Additionally, positive correlations between the expression of HOXC6 and the migration and proliferation of GBM cells were observed in vitro. The mechanistic analyses indicated that HOXC6 exerts its promotive effect on the progression and invasion of glioma cells by promoting the activation of the EMT and TGF-β/Smad signaling pathways. Conclusions. HOXC6 enhances the migration and proliferation of GBM by activating the EMT signaling pathway.</description><subject>Analysis</subject><subject>Apoptosis</subject><subject>Blood diseases</subject><subject>Brain cancer</subject><subject>Cancer</subject><subject>Chemotherapy</subject><subject>Gene expression</subject><subject>Genes</subject><subject>Genetic aspects</subject><subject>Genetic transcription</subject><subject>Gliomas</subject><subject>Growth factors</subject><subject>Immunohistochemistry</subject><subject>Medical prognosis</subject><subject>Metastasis</subject><subject>Nervous system</subject><subject>Prognosis</subject><subject>Radiation therapy</subject><subject>Stem cells</subject><subject>Transcription factors</subject><subject>Transforming growth factors</subject><subject>Tumors</subject><subject>Wound healing</subject><issn>1687-8450</issn><issn>1687-8450</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><sourceid>RHX</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><recordid>eNp90s9u0zAcB_AIgdgY3DgjS1yQINRObCe5IE3V1iENrWJF4mb94jiJJ8cudsLUh9jL7EF4Jty1TIUDp58tf_T1v1-SvCb4IyGMzTKcZbMSE05w9iQ5Jrws0pIy_PRgfJS8COEGY05xxZ8nRzljBaEVOU7uLq6-zzn6qrrJwKgCGnuFztY6FqPBpF9UUFb2mwEMWnmwQY_a2ai8m7r-Qa8W5-mv-9n1AA261p0Fo22HljD2t7BBYBu09KrRcgwI0NI5H-eusy7ogLRFC6NdbSCMboCXybMWTFCv9vUk-XZ-tppfpJdXi8_z08tU0oKPaa44VAANy6mUFc6brATSMEkVyRtZklq2dZHJlsoCA6k4rquaRVhURFFesfwk-bTLXU_1oBqp7OjBiLXXA_iNcKDF3ytW96JzP0WFqzLPSQx4tw_w7sekwigGHaQyBqxyUxAZ54xgmhVFpG__oTdu8vGVHhTlpMT0QHVglNC2dXFfuQ0VpwXOS5Yxmkf1YaekdyF41T4emWCx7Qax7Qax74bI3xxe8xH_-f4I3u9Ar20Dt_r_cb8BI6e9lA</recordid><startdate>20220505</startdate><enddate>20220505</enddate><creator>Eryi, Sun</creator><creator>Zheng, Li</creator><creator>Honghua, Cai</creator><creator>Su, Zhao</creator><creator>Han, Xie</creator><creator>Donggang, Pan</creator><creator>Zhou, Zhou</creator><creator>Liping, Zhan</creator><creator>Bo, Chen</creator><general>Hindawi</general><general>John Wiley & Sons, Inc</general><general>Hindawi Limited</general><scope>RHU</scope><scope>RHW</scope><scope>RHX</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7RV</scope><scope>7X7</scope><scope>7XB</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>KB0</scope><scope>M0S</scope><scope>NAPCQ</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0003-1756-5000</orcidid><orcidid>https://orcid.org/0000-0002-6772-1246</orcidid></search><sort><creationdate>20220505</creationdate><title>HOXC6 Regulates the Epithelial-Mesenchymal Transition through the TGF-β/Smad Signaling Pathway and Predicts a Poor Prognosis in Glioblastoma</title><author>Eryi, Sun ; Zheng, Li ; Honghua, Cai ; Su, Zhao ; Han, Xie ; Donggang, Pan ; Zhou, Zhou ; Liping, Zhan ; Bo, Chen</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c476t-3e6a9aad534cc903d28a1d5c4e13dc81bcfb72cf4c70a1960b9b5c90791e46953</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>Analysis</topic><topic>Apoptosis</topic><topic>Blood diseases</topic><topic>Brain cancer</topic><topic>Cancer</topic><topic>Chemotherapy</topic><topic>Gene expression</topic><topic>Genes</topic><topic>Genetic aspects</topic><topic>Genetic transcription</topic><topic>Gliomas</topic><topic>Growth factors</topic><topic>Immunohistochemistry</topic><topic>Medical prognosis</topic><topic>Metastasis</topic><topic>Nervous system</topic><topic>Prognosis</topic><topic>Radiation therapy</topic><topic>Stem cells</topic><topic>Transcription factors</topic><topic>Transforming growth factors</topic><topic>Tumors</topic><topic>Wound healing</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Eryi, Sun</creatorcontrib><creatorcontrib>Zheng, Li</creatorcontrib><creatorcontrib>Honghua, Cai</creatorcontrib><creatorcontrib>Su, Zhao</creatorcontrib><creatorcontrib>Han, Xie</creatorcontrib><creatorcontrib>Donggang, Pan</creatorcontrib><creatorcontrib>Zhou, Zhou</creatorcontrib><creatorcontrib>Liping, Zhan</creatorcontrib><creatorcontrib>Bo, Chen</creatorcontrib><collection>Hindawi Publishing Complete</collection><collection>Hindawi Publishing Subscription Journals</collection><collection>Hindawi Publishing Open Access</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Nursing & Allied Health Database</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</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 Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Nursing & Allied Health Premium</collection><collection>Publicly Available Content 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 oncology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Eryi, Sun</au><au>Zheng, Li</au><au>Honghua, Cai</au><au>Su, Zhao</au><au>Han, Xie</au><au>Donggang, Pan</au><au>Zhou, Zhou</au><au>Liping, Zhan</au><au>Bo, Chen</au><au>Wang, Jimei</au><au>Jimei Wang</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>HOXC6 Regulates the Epithelial-Mesenchymal Transition through the TGF-β/Smad Signaling Pathway and Predicts a Poor Prognosis in Glioblastoma</atitle><jtitle>Journal of oncology</jtitle><addtitle>J Oncol</addtitle><date>2022-05-05</date><risdate>2022</risdate><volume>2022</volume><spage>8016102</spage><epage>18</epage><pages>8016102-18</pages><issn>1687-8450</issn><eissn>1687-8450</eissn><abstract>Background. The HOX gene family of transcription factors, characterized by conserved homeodomains, is positively correlated with the resistance to chemotherapy drugs and poor prognosis, as well as the initiating potential of gliomas. However, there are few studies regarding the HOXC6 gene in glioma cells. Therefore, in the present study, we explored the regulatory roles and detailed mechanisms underlying the relationship between HOXC6 and the progression of GBM. Methods. The expression levels and prognostic value of HOXC6 in GBM were evaluated using the data obtained from the GCCA, GEPIA, and ONCOMINE databases. The relationship between GBM prognosis and levels of HOXC6 was identified using Kaplan-Meier curves. The protein levels of HOXC6 in GBM and adjacent normal tissues were identified via Western blot and immunohistochemistry (IHC) staining methods. Lentiviruses containing full-length HOXC6 and HOXC6 specific siRNA sequences were used to overexpress and knock down, respectively, the expression of HOXC6 in U87 and U251 cells. The role of HOXC6 in the regulation of migration and proliferation of GBM cells was accessed using Transwell, wound healing, CCK-8, and colony formation assays. The activation of the TGF-β/Smad signaling pathway was detected via Western blotting. Results. Compared to normal tissues and control cells, GBM tissues and cell lines showed higher expressions of HOXC6. The expression of HOXC6 was associated with disease-free and the overall survival of GBM patients. Additionally, positive correlations between the expression of HOXC6 and the migration and proliferation of GBM cells were observed in vitro. The mechanistic analyses indicated that HOXC6 exerts its promotive effect on the progression and invasion of glioma cells by promoting the activation of the EMT and TGF-β/Smad signaling pathways. Conclusions. HOXC6 enhances the migration and proliferation of GBM by activating the EMT signaling pathway.</abstract><cop>Egypt</cop><pub>Hindawi</pub><pmid>35571491</pmid><doi>10.1155/2022/8016102</doi><tpages>18</tpages><orcidid>https://orcid.org/0000-0003-1756-5000</orcidid><orcidid>https://orcid.org/0000-0002-6772-1246</orcidid><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1687-8450 |
| ispartof | Journal of oncology, 2022-05, Vol.2022, p.8016102-18 |
| issn | 1687-8450 1687-8450 |
| language | eng |
| recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_9098331 |
| source | Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central Open Access; Wiley Online Library Open Access; PubMed Central; Alma/SFX Local Collection |
| subjects | Analysis Apoptosis Blood diseases Brain cancer Cancer Chemotherapy Gene expression Genes Genetic aspects Genetic transcription Gliomas Growth factors Immunohistochemistry Medical prognosis Metastasis Nervous system Prognosis Radiation therapy Stem cells Transcription factors Transforming growth factors Tumors Wound healing |
| title | HOXC6 Regulates the Epithelial-Mesenchymal Transition through the TGF-β/Smad Signaling Pathway and Predicts a Poor Prognosis in Glioblastoma |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-18T11%3A20%3A31IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=HOXC6%20Regulates%20the%20Epithelial-Mesenchymal%20Transition%20through%20the%20TGF-%CE%B2/Smad%20Signaling%20Pathway%20and%20Predicts%20a%20Poor%20Prognosis%20in%20Glioblastoma&rft.jtitle=Journal%20of%20oncology&rft.au=Eryi,%20Sun&rft.date=2022-05-05&rft.volume=2022&rft.spage=8016102&rft.epage=18&rft.pages=8016102-18&rft.issn=1687-8450&rft.eissn=1687-8450&rft_id=info:doi/10.1155/2022/8016102&rft_dat=%3Cgale_pubme%3EA703852543%3C/gale_pubme%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2664618047&rft_id=info:pmid/35571491&rft_galeid=A703852543&rfr_iscdi=true |