Hexokinase 2 Regulates Ovarian Cancer Cell Migration, Invasion and Stemness via FAK/ERK1/2/MMP9/NANOG/SOX9 Signaling Cascades
Metabolic reprogramming is a common phenomenon in cancers. Thus, glycolytic enzymes could be exploited to selectively target cancer cells in cancer therapy. Hexokinase 2 (HK2) converts glucose to glucose-6-phosphate, the first committed step in glucose metabolism. Here, we demonstrated that HK2 was...
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| Veröffentlicht in: | Cancers 2019-06, Vol.11 (6), p.813 |
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| creator | Siu, Michelle K Y Jiang, Yu-Xin Wang, Jing-Jing Leung, Thomas H Y Han, Chae Young Tsang, Benjamin K Cheung, Annie N Y Ngan, Hextan Y S Chan, Karen K L |
| description | Metabolic reprogramming is a common phenomenon in cancers. Thus, glycolytic enzymes could be exploited to selectively target cancer cells in cancer therapy. Hexokinase 2 (HK2) converts glucose to glucose-6-phosphate, the first committed step in glucose metabolism. Here, we demonstrated that HK2 was overexpressed in ovarian cancer and displayed significantly higher expression in ascites and metastatic foci. HK2 expression was significantly associated with advanced stage and high-grade cancers, and was an independent prognostic factor. Functionally, knockdown of HK2 in ovarian cancer cell lines and ascites-derived tumor cells hindered lactate production, cell migration and invasion, and cell stemness properties, along with reduced FAK/ERK1/2 activation and metastasis- and stemness-related genes. 2-DG, a glycolysis inhibitor, retarded cell migration and invasion and reduced stemness properties. Inversely, overexpression of HK2 promoted cell migration and invasion through the FAK/ERK1/2/MMP9 pathway, and enhanced stemness properties via the FAK/ERK1/2/NANOG/SOX9 cascade. HK2 abrogation impeded in vivo tumor growth and dissemination. Notably, ovarian cancer-associated fibroblast-derived IL-6 contributed to its up-regulation. In conclusion, HK2, which is regulated by the tumor microenvironment, controls lactate production and contributes to ovarian cancer metastasis and stemness regulation via FAK/ERK1/2 signaling pathway-mediated MMP9/NANOG/SOX9 expression. HK2 could be a potential prognostic marker and therapeutic target for ovarian cancer. |
| doi_str_mv | 10.3390/cancers11060813 |
| format | Article |
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Thus, glycolytic enzymes could be exploited to selectively target cancer cells in cancer therapy. Hexokinase 2 (HK2) converts glucose to glucose-6-phosphate, the first committed step in glucose metabolism. Here, we demonstrated that HK2 was overexpressed in ovarian cancer and displayed significantly higher expression in ascites and metastatic foci. HK2 expression was significantly associated with advanced stage and high-grade cancers, and was an independent prognostic factor. Functionally, knockdown of HK2 in ovarian cancer cell lines and ascites-derived tumor cells hindered lactate production, cell migration and invasion, and cell stemness properties, along with reduced FAK/ERK1/2 activation and metastasis- and stemness-related genes. 2-DG, a glycolysis inhibitor, retarded cell migration and invasion and reduced stemness properties. Inversely, overexpression of HK2 promoted cell migration and invasion through the FAK/ERK1/2/MMP9 pathway, and enhanced stemness properties via the FAK/ERK1/2/NANOG/SOX9 cascade. HK2 abrogation impeded in vivo tumor growth and dissemination. Notably, ovarian cancer-associated fibroblast-derived IL-6 contributed to its up-regulation. In conclusion, HK2, which is regulated by the tumor microenvironment, controls lactate production and contributes to ovarian cancer metastasis and stemness regulation via FAK/ERK1/2 signaling pathway-mediated MMP9/NANOG/SOX9 expression. HK2 could be a potential prognostic marker and therapeutic target for ovarian cancer.</description><identifier>ISSN: 2072-6694</identifier><identifier>EISSN: 2072-6694</identifier><identifier>DOI: 10.3390/cancers11060813</identifier><identifier>PMID: 31212816</identifier><language>eng</language><publisher>Switzerland: MDPI AG</publisher><subject>Ascites ; Breast cancer ; Cancer ; Cancer therapies ; Care and treatment ; Cell activation ; Cell adhesion & migration ; Cell migration ; Chemotherapy ; Development and progression ; Dextrose ; Enzymes ; Extracellular signal-regulated kinase ; Focal adhesion kinase ; Gelatinase B ; Genes ; Glucose ; Glucose metabolism ; Glycolysis ; Gynecology ; Health aspects ; Hexokinase ; Interleukin 6 ; Kinases ; Lactates ; Lactic acid ; Medical prognosis ; Metabolism ; Metastases ; Metastasis ; Obstetrics ; Ovarian cancer ; Phosphates ; Prognosis ; Proteins ; Signal transduction ; Sox9 protein ; Therapeutic applications ; Therapeutic targets ; Transcription activation ; Tumor cell lines ; Tumor cells ; Tumor microenvironment ; Tumors ; Vascular endothelial growth factor</subject><ispartof>Cancers, 2019-06, Vol.11 (6), p.813</ispartof><rights>COPYRIGHT 2019 MDPI AG</rights><rights>2019. This work is licensed under https://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>2019 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2019 by the authors. 2019</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4583-d2bad2898d1ee4f9cd2d174f76a2b9bdffc9d58af46da126d550cfbf18036b2f3</citedby><cites>FETCH-LOGICAL-c4583-d2bad2898d1ee4f9cd2d174f76a2b9bdffc9d58af46da126d550cfbf18036b2f3</cites><orcidid>0000-0002-1584-7568 ; 0000-0002-4034-7469 ; 0000-0003-3945-159X</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/PMC6627345/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6627345/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31212816$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Siu, Michelle K Y</creatorcontrib><creatorcontrib>Jiang, Yu-Xin</creatorcontrib><creatorcontrib>Wang, Jing-Jing</creatorcontrib><creatorcontrib>Leung, Thomas H Y</creatorcontrib><creatorcontrib>Han, Chae Young</creatorcontrib><creatorcontrib>Tsang, Benjamin K</creatorcontrib><creatorcontrib>Cheung, Annie N Y</creatorcontrib><creatorcontrib>Ngan, Hextan Y S</creatorcontrib><creatorcontrib>Chan, Karen K L</creatorcontrib><title>Hexokinase 2 Regulates Ovarian Cancer Cell Migration, Invasion and Stemness via FAK/ERK1/2/MMP9/NANOG/SOX9 Signaling Cascades</title><title>Cancers</title><addtitle>Cancers (Basel)</addtitle><description>Metabolic reprogramming is a common phenomenon in cancers. Thus, glycolytic enzymes could be exploited to selectively target cancer cells in cancer therapy. Hexokinase 2 (HK2) converts glucose to glucose-6-phosphate, the first committed step in glucose metabolism. Here, we demonstrated that HK2 was overexpressed in ovarian cancer and displayed significantly higher expression in ascites and metastatic foci. HK2 expression was significantly associated with advanced stage and high-grade cancers, and was an independent prognostic factor. Functionally, knockdown of HK2 in ovarian cancer cell lines and ascites-derived tumor cells hindered lactate production, cell migration and invasion, and cell stemness properties, along with reduced FAK/ERK1/2 activation and metastasis- and stemness-related genes. 2-DG, a glycolysis inhibitor, retarded cell migration and invasion and reduced stemness properties. Inversely, overexpression of HK2 promoted cell migration and invasion through the FAK/ERK1/2/MMP9 pathway, and enhanced stemness properties via the FAK/ERK1/2/NANOG/SOX9 cascade. HK2 abrogation impeded in vivo tumor growth and dissemination. Notably, ovarian cancer-associated fibroblast-derived IL-6 contributed to its up-regulation. In conclusion, HK2, which is regulated by the tumor microenvironment, controls lactate production and contributes to ovarian cancer metastasis and stemness regulation via FAK/ERK1/2 signaling pathway-mediated MMP9/NANOG/SOX9 expression. HK2 could be a potential prognostic marker and therapeutic target for ovarian cancer.</description><subject>Ascites</subject><subject>Breast cancer</subject><subject>Cancer</subject><subject>Cancer therapies</subject><subject>Care and treatment</subject><subject>Cell activation</subject><subject>Cell adhesion & migration</subject><subject>Cell migration</subject><subject>Chemotherapy</subject><subject>Development and progression</subject><subject>Dextrose</subject><subject>Enzymes</subject><subject>Extracellular signal-regulated kinase</subject><subject>Focal adhesion kinase</subject><subject>Gelatinase B</subject><subject>Genes</subject><subject>Glucose</subject><subject>Glucose metabolism</subject><subject>Glycolysis</subject><subject>Gynecology</subject><subject>Health aspects</subject><subject>Hexokinase</subject><subject>Interleukin 6</subject><subject>Kinases</subject><subject>Lactates</subject><subject>Lactic acid</subject><subject>Medical prognosis</subject><subject>Metabolism</subject><subject>Metastases</subject><subject>Metastasis</subject><subject>Obstetrics</subject><subject>Ovarian cancer</subject><subject>Phosphates</subject><subject>Prognosis</subject><subject>Proteins</subject><subject>Signal transduction</subject><subject>Sox9 protein</subject><subject>Therapeutic applications</subject><subject>Therapeutic targets</subject><subject>Transcription activation</subject><subject>Tumor cell lines</subject><subject>Tumor cells</subject><subject>Tumor microenvironment</subject><subject>Tumors</subject><subject>Vascular endothelial growth factor</subject><issn>2072-6694</issn><issn>2072-6694</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>8G5</sourceid><sourceid>BENPR</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNp9kstv1DAQxiMEolXpmRuyxIUDS-Kx49gXpNWqL7XbRV2QuFkTP4JL1ilxsoJD__emtJTSA3PxSP7NNw99WfaaFh8YU0VuMBrXJ0oLUUjKnmW7UFQwE0Lx54_ynWw_pctiCsZoJaqX2Q6jQEFSsZtdH7uf3fcQMTkC5MI1Y4uDS2S1xT5gJIvfPcjCtS1ZhqbHIXTxPTmJW0xTRjBash7cJrqUyDYgOZyf5gcXpzSHfLn8pPLz-fnqKF-vviqyDk3ENsRmUk0GrUuvshce2-T279-97MvhwefF8exsdXSymJ_NDC8lm1mo0YJU0lLnuFfGgqUV95VAqFVtvTfKlhI9FxYpCFuWhfG1p7JgogbP9rKPd7pXY71x1rg49Njqqz5ssP-lOwz6358Yvumm22ohoGK8nATe3Qv03Y_RpUFvQjLTUTC6bkwagDOuZAlqQt8-QS-7sZ8WT5pRLnglGIf_UQBKSAZlVf6lGmydDtF303TmtrWeSyh4pUrFJyq_o0zfpdQ7_7AYLfStU_QTp0wVbx7f44H_4wt2A2cht_k</recordid><startdate>20190612</startdate><enddate>20190612</enddate><creator>Siu, Michelle K Y</creator><creator>Jiang, Yu-Xin</creator><creator>Wang, Jing-Jing</creator><creator>Leung, Thomas H Y</creator><creator>Han, Chae Young</creator><creator>Tsang, Benjamin K</creator><creator>Cheung, Annie N Y</creator><creator>Ngan, Hextan Y S</creator><creator>Chan, Karen K L</creator><general>MDPI AG</general><general>MDPI</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7T5</scope><scope>7TO</scope><scope>7XB</scope><scope>8FE</scope><scope>8FH</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>H94</scope><scope>HCIFZ</scope><scope>LK8</scope><scope>M2O</scope><scope>M7P</scope><scope>MBDVC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-1584-7568</orcidid><orcidid>https://orcid.org/0000-0002-4034-7469</orcidid><orcidid>https://orcid.org/0000-0003-3945-159X</orcidid></search><sort><creationdate>20190612</creationdate><title>Hexokinase 2 Regulates Ovarian Cancer Cell Migration, Invasion and Stemness via FAK/ERK1/2/MMP9/NANOG/SOX9 Signaling Cascades</title><author>Siu, Michelle K Y ; Jiang, Yu-Xin ; Wang, Jing-Jing ; Leung, Thomas H Y ; Han, Chae Young ; Tsang, Benjamin K ; Cheung, Annie N Y ; Ngan, Hextan Y S ; Chan, Karen K L</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4583-d2bad2898d1ee4f9cd2d174f76a2b9bdffc9d58af46da126d550cfbf18036b2f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Ascites</topic><topic>Breast cancer</topic><topic>Cancer</topic><topic>Cancer therapies</topic><topic>Care and treatment</topic><topic>Cell activation</topic><topic>Cell adhesion & migration</topic><topic>Cell migration</topic><topic>Chemotherapy</topic><topic>Development and progression</topic><topic>Dextrose</topic><topic>Enzymes</topic><topic>Extracellular signal-regulated kinase</topic><topic>Focal adhesion kinase</topic><topic>Gelatinase B</topic><topic>Genes</topic><topic>Glucose</topic><topic>Glucose metabolism</topic><topic>Glycolysis</topic><topic>Gynecology</topic><topic>Health aspects</topic><topic>Hexokinase</topic><topic>Interleukin 6</topic><topic>Kinases</topic><topic>Lactates</topic><topic>Lactic acid</topic><topic>Medical prognosis</topic><topic>Metabolism</topic><topic>Metastases</topic><topic>Metastasis</topic><topic>Obstetrics</topic><topic>Ovarian cancer</topic><topic>Phosphates</topic><topic>Prognosis</topic><topic>Proteins</topic><topic>Signal transduction</topic><topic>Sox9 protein</topic><topic>Therapeutic applications</topic><topic>Therapeutic targets</topic><topic>Transcription activation</topic><topic>Tumor cell lines</topic><topic>Tumor cells</topic><topic>Tumor microenvironment</topic><topic>Tumors</topic><topic>Vascular endothelial growth factor</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Siu, Michelle K Y</creatorcontrib><creatorcontrib>Jiang, Yu-Xin</creatorcontrib><creatorcontrib>Wang, Jing-Jing</creatorcontrib><creatorcontrib>Leung, Thomas H Y</creatorcontrib><creatorcontrib>Han, Chae Young</creatorcontrib><creatorcontrib>Tsang, Benjamin K</creatorcontrib><creatorcontrib>Cheung, Annie N Y</creatorcontrib><creatorcontrib>Ngan, Hextan Y S</creatorcontrib><creatorcontrib>Chan, Karen K L</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Immunology Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Biological Science Collection</collection><collection>Research Library</collection><collection>Biological Science Database</collection><collection>Research Library (Corporate)</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>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Cancers</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Siu, Michelle K Y</au><au>Jiang, Yu-Xin</au><au>Wang, Jing-Jing</au><au>Leung, Thomas H Y</au><au>Han, Chae Young</au><au>Tsang, Benjamin K</au><au>Cheung, Annie N Y</au><au>Ngan, Hextan Y S</au><au>Chan, Karen K L</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Hexokinase 2 Regulates Ovarian Cancer Cell Migration, Invasion and Stemness via FAK/ERK1/2/MMP9/NANOG/SOX9 Signaling Cascades</atitle><jtitle>Cancers</jtitle><addtitle>Cancers (Basel)</addtitle><date>2019-06-12</date><risdate>2019</risdate><volume>11</volume><issue>6</issue><spage>813</spage><pages>813-</pages><issn>2072-6694</issn><eissn>2072-6694</eissn><abstract>Metabolic reprogramming is a common phenomenon in cancers. Thus, glycolytic enzymes could be exploited to selectively target cancer cells in cancer therapy. Hexokinase 2 (HK2) converts glucose to glucose-6-phosphate, the first committed step in glucose metabolism. Here, we demonstrated that HK2 was overexpressed in ovarian cancer and displayed significantly higher expression in ascites and metastatic foci. HK2 expression was significantly associated with advanced stage and high-grade cancers, and was an independent prognostic factor. Functionally, knockdown of HK2 in ovarian cancer cell lines and ascites-derived tumor cells hindered lactate production, cell migration and invasion, and cell stemness properties, along with reduced FAK/ERK1/2 activation and metastasis- and stemness-related genes. 2-DG, a glycolysis inhibitor, retarded cell migration and invasion and reduced stemness properties. Inversely, overexpression of HK2 promoted cell migration and invasion through the FAK/ERK1/2/MMP9 pathway, and enhanced stemness properties via the FAK/ERK1/2/NANOG/SOX9 cascade. HK2 abrogation impeded in vivo tumor growth and dissemination. Notably, ovarian cancer-associated fibroblast-derived IL-6 contributed to its up-regulation. In conclusion, HK2, which is regulated by the tumor microenvironment, controls lactate production and contributes to ovarian cancer metastasis and stemness regulation via FAK/ERK1/2 signaling pathway-mediated MMP9/NANOG/SOX9 expression. HK2 could be a potential prognostic marker and therapeutic target for ovarian cancer.</abstract><cop>Switzerland</cop><pub>MDPI AG</pub><pmid>31212816</pmid><doi>10.3390/cancers11060813</doi><orcidid>https://orcid.org/0000-0002-1584-7568</orcidid><orcidid>https://orcid.org/0000-0002-4034-7469</orcidid><orcidid>https://orcid.org/0000-0003-3945-159X</orcidid><oa>free_for_read</oa></addata></record> |
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| source | MDPI - Multidisciplinary Digital Publishing Institute; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central; PubMed Central Open Access |
| subjects | Ascites Breast cancer Cancer Cancer therapies Care and treatment Cell activation Cell adhesion & migration Cell migration Chemotherapy Development and progression Dextrose Enzymes Extracellular signal-regulated kinase Focal adhesion kinase Gelatinase B Genes Glucose Glucose metabolism Glycolysis Gynecology Health aspects Hexokinase Interleukin 6 Kinases Lactates Lactic acid Medical prognosis Metabolism Metastases Metastasis Obstetrics Ovarian cancer Phosphates Prognosis Proteins Signal transduction Sox9 protein Therapeutic applications Therapeutic targets Transcription activation Tumor cell lines Tumor cells Tumor microenvironment Tumors Vascular endothelial growth factor |
| title | Hexokinase 2 Regulates Ovarian Cancer Cell Migration, Invasion and Stemness via FAK/ERK1/2/MMP9/NANOG/SOX9 Signaling Cascades |
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