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- W2990280798 abstract "The remarkable cellular and genetic heterogeneity of soft tissue sarcomas (STSs) limits the clinical benefit of targeted therapies. Here, we show that expression of the gluconeogenic isozyme fructose-1,6-bisphosphatase 2 (FBP2) is silenced in a broad spectrum of sarcoma subtypes, revealing an apparent common metabolic feature shared by diverse STSs. Enforced FBP2 expression inhibits sarcoma cell and tumor growth through two distinct mechanisms. First, cytosolic FBP2 antagonizes elevated glycolysis associated with the “Warburg effect,” thereby inhibiting sarcoma cell proliferation. Second, nuclear-localized FBP2 restrains mitochondrial biogenesis and respiration in a catalytic-activity-independent manner by inhibiting the expression of nuclear respiratory factor and mitochondrial transcription factor A (TFAM). Specifically, nuclear FBP2 colocalizes with the c-Myc transcription factor at the TFAM locus and represses c-Myc-dependent TFAM expression. This unique dual function of FBP2 provides a rationale for its selective suppression in STSs, identifying a potential metabolic vulnerability of this malignancy and possible therapeutic target." @default.
- W2990280798 created "2019-12-05" @default.
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- W2990280798 date "2020-01-01" @default.
- W2990280798 modified "2023-10-16" @default.
- W2990280798 title "Fructose-1,6-Bisphosphatase 2 Inhibits Sarcoma Progression by Restraining Mitochondrial Biogenesis" @default.
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- W2990280798 doi "https://doi.org/10.1016/j.cmet.2019.10.012" @default.
- W2990280798 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/7301686" @default.
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- W2990280798 hasPublicationYear "2020" @default.
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