<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Dylgjeri E</submitter><funding>Cancer Research UK</funding><funding>HHS | NIH | National Cancer Institute</funding><funding>NCI NIH HHS</funding><funding>Prostate Cancer Foundation</funding><pagination>1446-1459</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9365345</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>28(7)</volume><pubmed_abstract>&lt;h4>Purpose&lt;/h4>DNA-dependent protein kinase catalytic subunit (DNA-PKcs, herein referred as DNA-PK) is a multifunctional kinase of high cancer relevance. DNA-PK is deregulated in multiple tumor types, including prostate cancer, and is associated with poor outcomes. DNA-PK was previously nominated as a therapeutic target and DNA-PK inhibitors are currently undergoing clinical investigation. Although DNA-PK is well studied in DNA repair and transcriptional regulation, much remains to be understood about the way by which DNA-PK drives aggressive disease phenotypes.&lt;h4>Experimental design&lt;/h4>Here, unbiased proteomic and metabolomic approaches in clinically relevant tumor models uncovered a novel role of DNA-PK in metabolic regulation of cancer progression. DNA-PK regulation of metabolism was</pubmed_abstract><journal>Clinical cancer research : an official journal of the American Association for Cancer Research</journal><pubmed_title>A Novel Role for DNA-PK in Metabolism by Regulating Glycolysis in Castration-Resistant Prostate Cancer.</pubmed_title><pmcid>PMC9365345</pmcid><funding_grant_id>20411</funding_grant_id><funding_grant_id>5R01CA18256905</funding_grant_id><funding_grant_id>P30 CA056036</funding_grant_id><funding_grant_id>F99CA212225</funding_grant_id><funding_grant_id>5R01CA17640105</funding_grant_id><funding_grant_id>F99 CA212225</funding_grant_id><pubmed_authors>Lallas CD</pubmed_authors><pubmed_authors>Holst J</pubmed_authors><pubmed_authors>McCue PA</pubmed_authors><pubmed_authors>Vasilevskaya I</pubmed_authors><pubmed_authors>Pang A</pubmed_authors><pubmed_authors>Dylgjeri E</pubmed_authors><pubmed_authors>Chand S</pubmed_authors><pubmed_authors>Butler LM</pubmed_authors><pubmed_authors>McNair CM</pubmed_authors><pubmed_authors>Shafi AA</pubmed_authors><pubmed_authors>Kothari V</pubmed_authors><pubmed_authors>Semenova G</pubmed_authors><pubmed_authors>Schiewer MJ</pubmed_authors><pubmed_authors>Gomella LG</pubmed_authors><pubmed_authors>Knudsen KE</pubmed_authors><pubmed_authors>Seifert EL</pubmed_authors><pubmed_authors>Kelly WK</pubmed_authors><pubmed_authors>Guan YF</pubmed_authors><pubmed_authors>Carroll JS</pubmed_authors><pubmed_authors>Gallagher PT</pubmed_authors><pubmed_authors>Goodwin JF</pubmed_authors><pubmed_authors>Mandigo AC</pubmed_authors><pubmed_authors>McCann JJ</pubmed_authors><pubmed_authors>Irani S</pubmed_authors></additional><is_claimable>false</is_claimable><name>A Novel Role for DNA-PK in Metabolism by Regulating Glycolysis in Castration-Resistant Prostate Cancer.</name><description>&lt;h4>Purpose&lt;/h4>DNA-dependent protein kinase catalytic subunit (DNA-PKcs, herein referred as DNA-PK) is a multifunctional kinase of high cancer relevance. DNA-PK is deregulated in multiple tumor types, including prostate cancer, and is associated with poor outcomes. DNA-PK was previously nominated as a therapeutic target and DNA-PK inhibitors are currently undergoing clinical investigation. Although DNA-PK is well studied in DNA repair and transcriptional regulation, much remains to be understood about the way by which DNA-PK drives aggressive disease phenotypes.&lt;h4>Experimental design&lt;/h4>Here, unbiased proteomic and metabolomic approaches in clinically relevant tumor models uncovered a novel role of DNA-PK in metabolic regulation of cancer progression. DNA-PK regulation of metabolism was</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 Apr</publication><modification>2025-04-22T04:27:49.611Z</modification><creation>2025-04-05T21:00:08.837Z</creation></dates><accession>S-EPMC9365345</accession><cross_references><pubmed>35078861</pubmed><doi>10.1158/1078-0432.CCR-21-1846</doi></cross_references></HashMap>