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PKM2

Extracellular PKM2 Facilitates Organ-Tissue Fibrosis Progression

[iScience] The authors reported that myofibroblasts expressed and secreted PKM2. Extracellular PKM2 upregulated arginase-1 expression in myofibroblasts, therefore facilitating proline biosynthesis and subsequent collagen production.

LNCAROD Enhances Hepatocellular Carcinoma Malignancy by Activating Glycolysis through Induction of Pyruvate Kinase Isoform PKM2

[Journal of Experimental & Clinical Cancer Research] Investigators found that LNCAROD was significantly upregulated and predicted a poorer prognosis in hepatocellular carcinoma (HCC) patients. LNCAROD significantly promoted HCC cell proliferation, migration, invasion, and chemoresistance both in vitro and in vivo.

SFPQ Promotes an Oncogenic Transcriptomic State in Melanoma

[Oncogene] Researchers reported that knockdown of splicing factor, proline- and glutamine-rich (SFPQ) expression in melanoma cells decelerated several cancer-associated cell phenotypes, including cell growth, migration, epithelial to mesenchymal transition, apoptosis, and glycolysis.

Differential Localization Patterns of Pyruvate Kinase Isoforms in Murine Naïve, Formative, and Primed Pluripotent States

[Experimental Cell Research] The authors characterized the cellular expression and localization patterns of pyruvate kinase muscle isoforms in mouse ESCs, chemically transitioned epiblast-like cells (mEpiLCs) representing formative pluripotency, and mEpiSCs using immunoblotting and confocal microscopy.

Dual Covalent Inhibition of PKM and IMPDH Targets Metabolism in Cutaneous Metastatic Melanoma

[Cancer Research] Scientists identified a drug, HA344, that concomitantly targets two distinct metabolic hubs in cancer cells.

PKM2-Dependent Metabolic Skewing of Hepatic Th17 Cells Regulates Pathogenesis of Non-alcoholic Fatty Liver Disease

[Cell Metabolism] Scientists uncovered and characterized a distinct population of inflammatory hepatic CXCR3+Th17 (ihTh17) cells sufficient to exacerbate non-alcoholic fatty liver disease pathogenesis.

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