Please use this identifier to cite or link to this item: http://cmuir.cmu.ac.th/jspui/handle/6653943832/75776
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dc.contributor.authorChalaithorn Nantasuphaen_US
dc.contributor.authorChanisa Thonusinen_US
dc.contributor.authorKittipat Charoenkwanen_US
dc.contributor.authorSiriporn Chattipakornen_US
dc.contributor.authorNipon Chattipakornen_US
dc.date.accessioned2022-10-16T07:02:37Z-
dc.date.available2022-10-16T07:02:37Z-
dc.date.issued2021-01-01en_US
dc.identifier.issn19438141en_US
dc.identifier.other2-s2.0-85116325253en_US
dc.identifier.urihttps://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=85116325253&origin=inwarden_US
dc.identifier.urihttp://cmuir.cmu.ac.th/jspui/handle/6653943832/75776-
dc.description.abstractCancer cells usually show adaptations to their metabolism that facilitate their growth, invasiveness, and metastasis. Therefore, reprogramming the energy metabolism is one of the current key foci of cancer research and treatment. Although aerobic glycolysis-the Warburg effect-has been thought to be the dominant energy metabolism in cancer, recent data indicate a different possibility, specifically that oxidative phosphorylation (OXPHOS) is the more likely form of energy metabolism in some cancer cells. Due to the heterogeneity of epithelial ovarian cancer, there are different metabolic preferences among cell types, study types (in vivo/in vitro), and invasiveness. Current knowledge acknowledges glycolysis to be the main energy provider in ovarian cancer growth, invasion, migration, and viability, so specific agents targeting the glycolysis or OXPHOS pathways have been used in previous studies to attenuate tumor progression and increase chemosensitization. However, chemoresistant cell lines exert various metabolic preferences. This review comprehensively summarizes the information from existing reports which could together provide an in-depth understanding and insights for the development of a novel targeted therapy which can be used as an adjunctive treatment to standard chemotherapy to decelerate tumor progression and decrease the epithelial ovarian cancer mortality rate.en_US
dc.subjectBiochemistry, Genetics and Molecular Biologyen_US
dc.titleMetabolic reprogramming in epithelial ovarian canceren_US
dc.typeJournalen_US
article.title.sourcetitleAmerican Journal of Translational Researchen_US
article.volume13en_US
article.stream.affiliationsChiang Mai Universityen_US
Appears in Collections:CMUL: Journal Articles

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