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  • Mutant IDH regulates glycogen metabolism from early cartilage development to malignant chondrosarcoma formation.

Mutant IDH regulates glycogen metabolism from early cartilage development to malignant chondrosarcoma formation.

Cell reports (2023-06-02)
Sinthu Pathmanapan, Raymond Poon, Tomasa Barrientos De Renshaw, Puviindran Nadesan, Makoto Nakagawa, Gireesh A Seesankar, Adrian Kwan Ho Loe, Hongyuan H Zhang, Joan J Guinovart, Jordi Duran, Christopher B Newgard, Jay S Wunder, Benjamin A Alman
ABSTRACT

Chondrosarcomas are the most common malignancy of cartilage and are associated with somatic mutations in isocitrate dehydrogenase 1 (IDH1) and IDH2 genes. Somatic IDH mutations are also found in its benign precursor lesion, enchondromas, suggesting that IDH mutations are early events in malignant transformation. Human mutant IDH chondrosarcomas and mutant Idh mice that develop enchondromas investigated in our studies display glycogen deposition exclusively in mutant cells from IDH mutant chondrosarcomas and Idh1 mutant murine growth plates. Pharmacologic blockade of glycogen utilization induces changes in tumor cell behavior, downstream energetic pathways, and tumor burden in vitro and in vivo. Mutant IDH1 interacts with hypoxia-inducible factor 1α (HIF1α) to regulate expression of key enzymes in glycogen metabolism. Here, we show a critical role for glycogen in enchondromas and chondrosarcomas, which is likely mediated through an interaction with mutant IDH1 and HIF1α.

MATERIALS
Product Number
Brand
Product Description

Sigma-Aldrich
Monoclonal Anti-β-Actin antibody produced in mouse, clone AC-74, purified immunoglobulin, buffered aqueous solution
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C28/I2 Human Chondrocyte Cell Line, C28/I2 Human Chondrocyte Cell Line is widely used as a model cell line for studying normal and pathological cartilage repair mechanisms related to chondrocyte biology and physiology.
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Tamoxifen, 4-Hydroxy-, (Z)-, A cell-permeable, active metabolite of Tamoxifen that acts as a potent inhibitor of PKC. It is more potent than the parent compound and inhibits PKC by modifying its catalytic domain.
Sigma-Aldrich
Anti-IDH1/2 Mutant (R132/172) Antibody, clone MsMab-1, clone MsMAb-1, from mouse