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Article: Targeting of lipid metabolism with a metabolic inhibitor cocktail eradicates peritoneal metastases in ovarian cancer cells

TitleTargeting of lipid metabolism with a metabolic inhibitor cocktail eradicates peritoneal metastases in ovarian cancer cells
Authors
Issue Date2019
PublisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/commsbio
Citation
Communications Biology, 2019, v. 2 n. 1, article no. 281 How to Cite?
AbstractOvarian cancer is an intra-abdominal tumor in which the presence of ascites facilitates metastatic dissemination, and associated with poor prognosis. However, the significance of metabolic alterations in ovarian cancer cells in the ascites microenvironment remains unclear. Here we show ovarian cancer cells exhibited increased aggressiveness in ascites microenvironment via reprogramming of lipid metabolism. High lipid metabolic activities are found in ovarian cancer cells when cultured in the ascites microenvironment, indicating a metabolic shift from aerobic glycolysis to β-oxidation and lipogenesis. The reduced AMP-activated protein kinase (AMPK) activity due to the feedback effect of high energy production led to the activation of its downstream signaling, which in turn, enhanced the cancer growth. The combined treatment of low toxic AMPK activators, the transforming growth factor beta-activated kinase 1 (TAK1) and fatty acid synthase (FASN) inhibitors synergistically impair oncogenic augmentation of ovarian cancer. Collectively, targeting lipid metabolism signaling axis impede ovarian cancer peritoneal metastases.
Persistent Identifierhttp://hdl.handle.net/10722/274459
ISSN

 

DC FieldValueLanguage
dc.contributor.authorChen, R-
dc.contributor.authorYung, MH-
dc.contributor.authorXuan, Y-
dc.contributor.authorZhan, S-
dc.contributor.authorLeung, LL-
dc.contributor.authorLiang, R-
dc.contributor.authorLeung, THY-
dc.contributor.authorYang, HJ-
dc.contributor.authorXu, D-
dc.contributor.authorSharma, R-
dc.contributor.authorChan, KKL-
dc.contributor.authorNgu, SF-
dc.contributor.authorNgan, HYS-
dc.contributor.authorChan, DW-
dc.date.accessioned2019-08-18T15:02:08Z-
dc.date.available2019-08-18T15:02:08Z-
dc.date.issued2019-
dc.identifier.citationCommunications Biology, 2019, v. 2 n. 1, article no. 281-
dc.identifier.issn2399-3642-
dc.identifier.urihttp://hdl.handle.net/10722/274459-
dc.description.abstractOvarian cancer is an intra-abdominal tumor in which the presence of ascites facilitates metastatic dissemination, and associated with poor prognosis. However, the significance of metabolic alterations in ovarian cancer cells in the ascites microenvironment remains unclear. Here we show ovarian cancer cells exhibited increased aggressiveness in ascites microenvironment via reprogramming of lipid metabolism. High lipid metabolic activities are found in ovarian cancer cells when cultured in the ascites microenvironment, indicating a metabolic shift from aerobic glycolysis to β-oxidation and lipogenesis. The reduced AMP-activated protein kinase (AMPK) activity due to the feedback effect of high energy production led to the activation of its downstream signaling, which in turn, enhanced the cancer growth. The combined treatment of low toxic AMPK activators, the transforming growth factor beta-activated kinase 1 (TAK1) and fatty acid synthase (FASN) inhibitors synergistically impair oncogenic augmentation of ovarian cancer. Collectively, targeting lipid metabolism signaling axis impede ovarian cancer peritoneal metastases.-
dc.languageeng-
dc.publisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/commsbio-
dc.relation.ispartofCommunications Biology-
dc.rightsThis work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.-
dc.titleTargeting of lipid metabolism with a metabolic inhibitor cocktail eradicates peritoneal metastases in ovarian cancer cells-
dc.typeArticle-
dc.identifier.emailYung, MH: mhyung@hku.hk-
dc.identifier.emailSharma, R: rasharma@hku.hk-
dc.identifier.emailChan, KKL: kklchan@hkucc.hku.hk-
dc.identifier.emailNgu, SF: ngusiewf@hku.hk-
dc.identifier.emailNgan, HYS: hysngan@hkucc.hku.hk-
dc.identifier.emailChan, DW: dwchan@hku.hk-
dc.identifier.authorityChan, KKL=rp00499-
dc.identifier.authorityNgu, SF=rp01367-
dc.identifier.authorityNgan, HYS=rp00346-
dc.identifier.authorityChan, DW=rp00543-
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.1038/s42003-019-0508-1-
dc.identifier.scopuseid_2-s2.0-85071151488  -
dc.identifier.hkuros301301-
dc.identifier.volume2-
dc.identifier.issue1-
dc.identifier.spagearticle no. 281-
dc.identifier.epagearticle no. 281-
dc.publisher.placeUnited Kingdom-

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