The oncoprotein HBXIP promotes glucose metabolism reprogramming via downregulating SCO2 and PDHA1 in breast cancer.

作者: Fabao Liu , Weiying Zhang , Xiaona You , Yunxia Liu , Yinghui Li

DOI: 10.18632/ONCOTARGET.4508

关键词:

摘要: The glucose metabolism reprogramming is a hallmark of cancer. oncoprotein hepatitis B X-interacting protein (HBXIP) functions in the development breast In this study, we supposed that HBXIP might be involved We showed led to increases generation intracellular and lactate, as well decreases reactive oxygen species. Expression synthesis cytochrome c oxidase 2 (SCO2) pyruvate dehydrogenase alpha 1 (PDHA1), two factors metabolic switch from oxidative phosphorylation aerobic glycolysis, was suppressed by HBXIP. addition, miR-183/182 miR-96 directly inhibited expression SCO2 PDHA1 through targeting their mRNA coding sequences (CDSs), respectively. Interestingly, elevated miR-183/96/182 cluster hypoxia-inducible factor 1α (HIF1α). stability HIF1α enhanced disassociating interaction von Hippel-Lindau (pVHL) with HIF1α. Moreover, miR-183 increased levels CDS VHL mRNA, forming feedback loop HIF1α/miR-183/pVHL/HIF1α. function, HBXIP-elevated vitro. HBXIP-triggered promoted growth cancer vivo. Thus, conclude enhances suppressing

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