Oncogenic metabolic reprogramming in breast cancer: focus on signaling pathways and mitochondrial genes

dc.contributor.authorMalayil, Rhuthuparna
dc.contributor.authorChhichholiya, Yogita
dc.contributor.authorVasudeva, Kanika
dc.contributor.authorSingh, Harsh Vikram
dc.contributor.authorSingh, Tashvinder
dc.contributor.authorSingh, Sandeep
dc.contributor.authorMunshi, Anjana
dc.date.accessioned2024-01-21T10:54:14Z
dc.date.accessioned2024-08-14T07:40:58Z
dc.date.available2024-01-21T10:54:14Z
dc.date.available2024-08-14T07:40:58Z
dc.date.issued2023-05-11T00:00:00
dc.description.abstractOncogenic metabolic reprogramming impacts the abundance of key metabolites that regulate signaling and epigenetics. Metabolic vulnerability in the cancer cell is evident from the Warburg effect. The research on metabolism in the progression and survival of breast cancer (BC) is under focus. Oncogenic signal activation and loss of�tumor suppressor are important regulators of tumor cell metabolism. Several intrinsic and extrinsic factors contribute to metabolic reprogramming. The molecular mechanisms underpinning metabolic reprogramming in BC are extensive and only partially defined. Various signaling pathways involved in the metabolism play a significant role in the modulation of BC. Notably, PI3K/AKT/mTOR pathway, lactate-ERK/STAT3 signaling, loss of the tumor suppressor Ras, Myc, oxidative stress, activation of the cellular hypoxic response and acidosis contribute to different metabolic reprogramming phenotypes linked to enhanced glycolysis. The alterations in mitochondrial genes have also been elaborated upon along with their functional implications. The outcome of these active research areas might contribute to the development of novel therapeutic interventions and the remodeling of known�drugs. � 2023, This is a U.S. Government work and not under copyright protection in the US; foreign copyright protection may apply.en_US
dc.identifier.doi10.1007/s12032-023-02037-2
dc.identifier.issn13570560
dc.identifier.urihttp://10.2.3.109/handle/32116/4253
dc.identifier.urlhttps://link.springer.com/10.1007/s12032-023-02037-2
dc.language.isoen_USen_US
dc.publisherSpringeren_US
dc.subjectBCen_US
dc.subjectMetabolic reprogrammingen_US
dc.subjectMitochondriaen_US
dc.subjectSignalingen_US
dc.titleOncogenic metabolic reprogramming in breast cancer: focus on signaling pathways and mitochondrial genesen_US
dc.title.journalMedical Oncologyen_US
dc.typeReviewen_US
dc.type.accesstypeClosed Accessen_US

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