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Cholesterol biosynthesis and mutant IDH activity are linked to cellular glycogen through PPP1R3C in growth plate chondrocytes and chondrosarcoma

ABSTRACT: Cholesterol biosynthesis and mutant IDH activity are linked to cellular glycogen through PPP1R3C in growth plate chondrocytes and chondrosarcoma

PROVIDER: PRJNA1124882 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR29433394_1.fastq.gz	Fastqsanger.gz
	SRR29433394_2.fastq.gz	Fastqsanger.gz
	SRR29433395_1.fastq.gz	Fastqsanger.gz
	SRR29433395_2.fastq.gz	Fastqsanger.gz
	SRR29433396_1.fastq.gz	Fastqsanger.gz

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Cholesterol biosynthesis and mutant IDH activity are linked to cellular glycogen through PPP1R3C in growth plate chondrocytes and chondrosarcoma

Project description:Enchondromas are common bone tumors composed of chondrocytes originating from growth plate cells, which can progress to malignant chondrosarcoma. Mutations in the genes encoding isocitrate dehydrogenase (IDH1 and IDH2) are identified in a large proportion of these tumors. IDH enzymes convert isocitrate to alpha-ketoglutarate (α-KG), an essential component of the citric acid cycle. The mutant IDH enzymes produce 2-hydroxyglutarate (2-HG), which has epigenetic effects important in tumor initiation. Tumor maintenance and growth rely on additional factors as well. Prior work shows that intracellular cholesterol and glycogen are upregulated in mutant IDH chondrocytes. Here, we show that Protein Phosphatase 1 Regulatory Subunit 3C (PPP1R3C, previously termed Protein Targeting to Glycogen or PTG) is upregulated in chondrocytes harboring a mutant IDH. PPP1R3C expression correlates with the level of intracellular cholesterol biosynthesis and can be regulated by Sterol Regulatory Element-Binding Proteins (SREBPs), which are transcriptional regulators of enzymes involved in sterol biosynthesis. We found that PPP1R3C regulates glycolysis and glycolytic capacity in chondrocytes. Depletion of PPP1R3C in mouse chondrocytes in vivo suppresses the enchondroma phenotype. The growth plate phenotype associated with the inhibition of cholesterol biosynthesis is partially rescued by PPP1R3C overexpression. Taken together, our data show that PPP1R3C integrates the effects of cholesterol metabolism and isocitrate dehydrogenase on growth plate and neoplastic chondrocyte metabolism by regulating intracellular glycogen levels.

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Cholesterol biosynthesis and mutant IDH activity are linked to cellular glycogen through PPP1R3C in growth plate chondrocytes and chondrosarcoma [RNA-seq]

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Cholesterol biosynthesis and mutant IDH activity are linked to cellular glycogen through PPP1R3C in growth plate chondrocytes and chondrosarcoma [RNA-seq]

Project description:Cholesterol biosynthesis and mutant IDH activity are linked to cellular glycogen through PPP1R3C in growth plate chondrocytes and chondrosarcoma [RNA-seq]

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Bovine Hypertrophic Growth Plate Chondrocytes vs. Reserve Zone Chondrocytes

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Gene expression profile at single vell level of growth plate chondrocytes [scRNA-seq]

Project description:Gowth plate chondrocytes include heterogenous cell population and cellular diversity of these chondrocytes remains to be elucidated. We used single cell RNA sequencing to uncover the diverssity of growth plate chondrocytes and identify noel marker genes selectively expressed in pre-hypertrophic chondrocytes.

2024-11-21 | GSE271634 | GEO

Transcription profiling of Bos taurus hypertrophic growth plate chondrocytes vs. reserve zone chondrocytes

Project description:Growth plate chondrocytes were isolated from the distal metacarpus of young dairy cattle (all under 10 mo of age), the chondrocytes were released from the extracellular matrix by digestion with Collagenase P for 4 hours, and the various zones of the growth plate were separated by density centrifugation. The least-dense Hypertrophic Zone (HZ) cells were compared to the most-dense Reserve Zone (RZ) cells. 6 pairs of HZ vs RZ were compared by microarray. Experiment Overall Design: Growth plate chondrocytes were isolated from the distal metacarpus of young dairy cattle (all under 10 mo of age), the chondrocytes were released from the extracellular matrix by digestion with Collagenase P for 4 hours, and the various zones of the growth plate were separated by density centrifugation. The least-dense Hypertrophic Zone (HZ) cells were compared to the most-dense Reserve Zone (RZ) cells. Six independent sample pairs of HZ vs RZ were compared by microarray.

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Project description:Mutations in isocitrate dehydrogenase (IDH) genes occur in various malignant tumors including chondrosarcoma. IDH mutations contribute to malignant transformation by catalyzing the production of 2-hydroxyglutarate (2-HG), a competitive inhibitor of α-ketoglutarate-dependent dioxygenases. Mutant IDH inhibitors are therefore potential novel anticancer drugs in IDH mutant tumors. Here, we examined the efficacy of the inhibition of mutant IDH1 as an antitumor approach in chondrosarcoma cells in vitro and in vivo, and investigated the association between the IDH mutation and chondrosarcoma cells.

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