Phosphorylation of FOXK2 at Thr13 and Ser30 by PDK2 sustains glycolysis through a positive feedback manner in ovarian cancer
Ovarian cancer is one of the most common gynecological malignant tumors with insidious onset, strong invasiveness, and poor prognosis. Metabolic alteration, particularly aerobic glycolysis, which is tightly regulated by transcription factors, is associated with the malignant behavior of OC. We scree...
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| Veröffentlicht in: | Oncogene 2024-06, Vol.43 (26), p.1985-1999 |
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| creator | Zhang, Cancan Xu, Yinyin Zhu, Xinyue Zhang, Xueli Wang, Fengmian Hu, Lipeng Lu, Huan Tao, Chunlin Xu, Kai Zhang, Zhigang Li, Dongxue Shi, Tingyan Zhang, Rong |
| description | Ovarian cancer is one of the most common gynecological malignant tumors with insidious onset, strong invasiveness, and poor prognosis. Metabolic alteration, particularly aerobic glycolysis, which is tightly regulated by transcription factors, is associated with the malignant behavior of OC. We screened FOXK2 in this study as a key transcription factor that regulates glycolysis in OC. FOXK2 is overly expressed in OC, and poor prognosis is predicted by overexpression. FOXK2 promotes OC cell proliferation both in vitro and in vivo and cell migration in vitro. Further studies showed that PDK2 directly binds to the forkhead-associated (FHA) domain of FOXK2 to phosphorylate FOXK2 at Thr13 and Ser30, thereby enhancing the transcriptional activity of FOXK2. FOXK2 transcriptionally regulates the expression of PDK2, thus forming positive feedback to sustain glycolysis in OC cells. |
| doi_str_mv | 10.1038/s41388-024-03052-x |
| format | Article |
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Metabolic alteration, particularly aerobic glycolysis, which is tightly regulated by transcription factors, is associated with the malignant behavior of OC. We screened FOXK2 in this study as a key transcription factor that regulates glycolysis in OC. FOXK2 is overly expressed in OC, and poor prognosis is predicted by overexpression. FOXK2 promotes OC cell proliferation both in vitro and in vivo and cell migration in vitro. Further studies showed that PDK2 directly binds to the forkhead-associated (FHA) domain of FOXK2 to phosphorylate FOXK2 at Thr13 and Ser30, thereby enhancing the transcriptional activity of FOXK2. FOXK2 transcriptionally regulates the expression of PDK2, thus forming positive feedback to sustain glycolysis in OC cells.</description><identifier>ISSN: 0950-9232</identifier><identifier>ISSN: 1476-5594</identifier><identifier>EISSN: 1476-5594</identifier><identifier>DOI: 10.1038/s41388-024-03052-x</identifier><identifier>PMID: 38734828</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>13/1 ; 13/51 ; 13/89 ; 38/1 ; 45/91 ; 631/67/1517/1709 ; 631/67/2327 ; 82/51 ; 82/80 ; Animals ; Apoptosis ; Cell adhesion & migration ; Cell Biology ; Cell growth ; Cell Line, Tumor ; Cell migration ; Cell Movement - genetics ; Cell proliferation ; Cell Proliferation - genetics ; Chemotherapy ; Cytokines ; Enzymes ; Feedback ; Feedback, Physiological ; Female ; Forkhead protein ; Forkhead Transcription Factors - genetics ; Forkhead Transcription Factors - metabolism ; Gene Expression Regulation, Neoplastic ; Genes ; Genomics ; Glucose ; Glycolysis ; Glycolysis - genetics ; Human Genetics ; Humans ; Internal Medicine ; Invasiveness ; Medical prognosis ; Medicine ; Medicine & Public Health ; Metabolism ; Metastasis ; Mice ; Mice, Nude ; Oncology ; Ovarian cancer ; Ovarian Neoplasms - genetics ; Ovarian Neoplasms - metabolism ; Ovarian Neoplasms - pathology ; Phosphorylation ; Prognosis ; Proteins ; Pyruvate Dehydrogenase Acetyl-Transferring Kinase - genetics ; Pyruvate Dehydrogenase Acetyl-Transferring Kinase - metabolism ; Transcription factors ; Tumorigenesis ; Tumors</subject><ispartof>Oncogene, 2024-06, Vol.43 (26), p.1985-1999</ispartof><rights>The Author(s) 2024</rights><rights>2024. The Author(s).</rights><rights>The Author(s) 2024. This work is published 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><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c426t-7e3a116401162aeab644e2b271e5f514b93bac31e82d4b65a54d05130a0ed1293</cites><orcidid>0000-0001-8306-0639 ; 0000-0001-8965-223X ; 0000-0002-5941-3825 ; 0000-0002-2136-7181</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,780,784,885,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/38734828$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhang, Cancan</creatorcontrib><creatorcontrib>Xu, Yinyin</creatorcontrib><creatorcontrib>Zhu, Xinyue</creatorcontrib><creatorcontrib>Zhang, Xueli</creatorcontrib><creatorcontrib>Wang, Fengmian</creatorcontrib><creatorcontrib>Hu, Lipeng</creatorcontrib><creatorcontrib>Lu, Huan</creatorcontrib><creatorcontrib>Tao, Chunlin</creatorcontrib><creatorcontrib>Xu, Kai</creatorcontrib><creatorcontrib>Zhang, Zhigang</creatorcontrib><creatorcontrib>Li, Dongxue</creatorcontrib><creatorcontrib>Shi, Tingyan</creatorcontrib><creatorcontrib>Zhang, Rong</creatorcontrib><title>Phosphorylation of FOXK2 at Thr13 and Ser30 by PDK2 sustains glycolysis through a positive feedback manner in ovarian cancer</title><title>Oncogene</title><addtitle>Oncogene</addtitle><addtitle>Oncogene</addtitle><description>Ovarian cancer is one of the most common gynecological malignant tumors with insidious onset, strong invasiveness, and poor prognosis. Metabolic alteration, particularly aerobic glycolysis, which is tightly regulated by transcription factors, is associated with the malignant behavior of OC. We screened FOXK2 in this study as a key transcription factor that regulates glycolysis in OC. FOXK2 is overly expressed in OC, and poor prognosis is predicted by overexpression. FOXK2 promotes OC cell proliferation both in vitro and in vivo and cell migration in vitro. Further studies showed that PDK2 directly binds to the forkhead-associated (FHA) domain of FOXK2 to phosphorylate FOXK2 at Thr13 and Ser30, thereby enhancing the transcriptional activity of FOXK2. FOXK2 transcriptionally regulates the expression of PDK2, thus forming positive feedback to sustain glycolysis in OC cells.</description><subject>13/1</subject><subject>13/51</subject><subject>13/89</subject><subject>38/1</subject><subject>45/91</subject><subject>631/67/1517/1709</subject><subject>631/67/2327</subject><subject>82/51</subject><subject>82/80</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>Cell adhesion & migration</subject><subject>Cell Biology</subject><subject>Cell growth</subject><subject>Cell Line, Tumor</subject><subject>Cell migration</subject><subject>Cell Movement - genetics</subject><subject>Cell proliferation</subject><subject>Cell Proliferation - genetics</subject><subject>Chemotherapy</subject><subject>Cytokines</subject><subject>Enzymes</subject><subject>Feedback</subject><subject>Feedback, Physiological</subject><subject>Female</subject><subject>Forkhead protein</subject><subject>Forkhead Transcription Factors - genetics</subject><subject>Forkhead Transcription Factors - metabolism</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Genes</subject><subject>Genomics</subject><subject>Glucose</subject><subject>Glycolysis</subject><subject>Glycolysis - genetics</subject><subject>Human Genetics</subject><subject>Humans</subject><subject>Internal Medicine</subject><subject>Invasiveness</subject><subject>Medical prognosis</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Metabolism</subject><subject>Metastasis</subject><subject>Mice</subject><subject>Mice, Nude</subject><subject>Oncology</subject><subject>Ovarian cancer</subject><subject>Ovarian Neoplasms - genetics</subject><subject>Ovarian Neoplasms - metabolism</subject><subject>Ovarian Neoplasms - pathology</subject><subject>Phosphorylation</subject><subject>Prognosis</subject><subject>Proteins</subject><subject>Pyruvate Dehydrogenase Acetyl-Transferring Kinase - genetics</subject><subject>Pyruvate Dehydrogenase Acetyl-Transferring Kinase - metabolism</subject><subject>Transcription factors</subject><subject>Tumorigenesis</subject><subject>Tumors</subject><issn>0950-9232</issn><issn>1476-5594</issn><issn>1476-5594</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><sourceid>C6C</sourceid><sourceid>EIF</sourceid><recordid>eNp9kUtv1DAUhS0EokPhD7BAltiwCVy_8lghVCggKrUSRWJn3SR3Ji4Ze7CTUSPx4zFMKY8FG3txvnuOrw9jjwU8F6DqF0kLVdcFSF2AAiOL6ztsJXRVFsY0-i5bQWOgaKSSR-xBSlcAUDUg77MjVVdK17JesW8XQ0i7IcRlxMkFz8Oan55__iA5TvxyiEJx9D3_SFEBbxd-8TpLaU4TOp_4Zly6MC7JJT4NMcybgSPfheQmtye-Jupb7L7wLXpPkbvsvsfo0PMOfUfxIbu3xjHRo5v7mH06fXN58q44O3_7_uTVWdFpWU5FRQqFKDXkQyJhW2pNspWVILM2QreNyjFKUC173ZYGje7BCAUI1AvZqGP28uC7m9st9R35KeJod9FtMS42oLN_K94NdhP2VgjRlFKY7PDsxiGGrzOlyW5d6mgc0VOYk83fr5oKclZGn_6DXoU5-rxfpipRKiUrmSl5oLoYUoq0vn2NAPujXXto1-Z27c927XUeevLnHrcjv-rMgDoAKUt-Q_F39n9svwONm7CJ</recordid><startdate>20240624</startdate><enddate>20240624</enddate><creator>Zhang, Cancan</creator><creator>Xu, Yinyin</creator><creator>Zhu, Xinyue</creator><creator>Zhang, Xueli</creator><creator>Wang, Fengmian</creator><creator>Hu, Lipeng</creator><creator>Lu, Huan</creator><creator>Tao, Chunlin</creator><creator>Xu, Kai</creator><creator>Zhang, Zhigang</creator><creator>Li, Dongxue</creator><creator>Shi, Tingyan</creator><creator>Zhang, Rong</creator><general>Nature Publishing Group UK</general><general>Nature Publishing Group</general><scope>C6C</scope><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>7TM</scope><scope>7TO</scope><scope>7U9</scope><scope>8FD</scope><scope>FR3</scope><scope>H94</scope><scope>K9.</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0001-8306-0639</orcidid><orcidid>https://orcid.org/0000-0001-8965-223X</orcidid><orcidid>https://orcid.org/0000-0002-5941-3825</orcidid><orcidid>https://orcid.org/0000-0002-2136-7181</orcidid></search><sort><creationdate>20240624</creationdate><title>Phosphorylation of FOXK2 at Thr13 and Ser30 by PDK2 sustains glycolysis through a positive feedback manner in ovarian cancer</title><author>Zhang, Cancan ; 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Metabolic alteration, particularly aerobic glycolysis, which is tightly regulated by transcription factors, is associated with the malignant behavior of OC. We screened FOXK2 in this study as a key transcription factor that regulates glycolysis in OC. FOXK2 is overly expressed in OC, and poor prognosis is predicted by overexpression. FOXK2 promotes OC cell proliferation both in vitro and in vivo and cell migration in vitro. Further studies showed that PDK2 directly binds to the forkhead-associated (FHA) domain of FOXK2 to phosphorylate FOXK2 at Thr13 and Ser30, thereby enhancing the transcriptional activity of FOXK2. FOXK2 transcriptionally regulates the expression of PDK2, thus forming positive feedback to sustain glycolysis in OC cells.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>38734828</pmid><doi>10.1038/s41388-024-03052-x</doi><tpages>15</tpages><orcidid>https://orcid.org/0000-0001-8306-0639</orcidid><orcidid>https://orcid.org/0000-0001-8965-223X</orcidid><orcidid>https://orcid.org/0000-0002-5941-3825</orcidid><orcidid>https://orcid.org/0000-0002-2136-7181</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | 13/1 13/51 13/89 38/1 45/91 631/67/1517/1709 631/67/2327 82/51 82/80 Animals Apoptosis Cell adhesion & migration Cell Biology Cell growth Cell Line, Tumor Cell migration Cell Movement - genetics Cell proliferation Cell Proliferation - genetics Chemotherapy Cytokines Enzymes Feedback Feedback, Physiological Female Forkhead protein Forkhead Transcription Factors - genetics Forkhead Transcription Factors - metabolism Gene Expression Regulation, Neoplastic Genes Genomics Glucose Glycolysis Glycolysis - genetics Human Genetics Humans Internal Medicine Invasiveness Medical prognosis Medicine Medicine & Public Health Metabolism Metastasis Mice Mice, Nude Oncology Ovarian cancer Ovarian Neoplasms - genetics Ovarian Neoplasms - metabolism Ovarian Neoplasms - pathology Phosphorylation Prognosis Proteins Pyruvate Dehydrogenase Acetyl-Transferring Kinase - genetics Pyruvate Dehydrogenase Acetyl-Transferring Kinase - metabolism Transcription factors Tumorigenesis Tumors |
| title | Phosphorylation of FOXK2 at Thr13 and Ser30 by PDK2 sustains glycolysis through a positive feedback manner in ovarian cancer |
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