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- W3194753208 abstract "The mechanisms by which mitochondrial metabolism supports cancer anabolism are still unclear. Here, we unexpectedly find that genetic and pharmacological inactivation of Pyruvate Dehydrogenase A1 (PDHA1), a subunit of pyruvate dehydrogenase complex (PDC) inhibits prostate cancer development in different mouse and human xenograft tumor models by affecting lipid biosynthesis. Mechanistically, we show that in prostate cancer, PDC localizes in both mitochondria and nucleus. While nuclear PDC controls the expression of Sterol regulatory element-binding transcription factor (SREBF) target genes by mediating histone acetylation, mitochondrial PDC provides cytosolic citrate for lipid synthesis in a coordinated effort to sustain anabolism. In line with this evidence, we find that PDHA1 and the PDC activator, Pyruvate dehydrogenase phosphatase 1 (PDP1), are frequently amplified and overexpressed at both gene and protein level in prostate tumors. Taken together, these findings demonstrate that both mitochondrial and nuclear PDC sustain prostate tumorigenesis by controlling lipid biosynthesis thereby pointing at this complex as a novel target for cancer therapy." @default.
- W3194753208 created "2021-08-30" @default.
- W3194753208 creator A5084978681 @default.
- W3194753208 date "2018-03-07" @default.
- W3194753208 modified "2023-09-27" @default.
- W3194753208 title "Molecular and Metabolic Characterization of Mitochondria Mediated Tumourigenesis in Prostate Cancer" @default.
- W3194753208 hasPublicationYear "2018" @default.
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