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Methylation Mediated Silencing of Protein Kinase C Zeta Induces Apoptosis Avoidance through ATM/Chk-2 Inactivation in Dedifferentiated Chondrosarcoma

ABSTRACT: Methylation Mediated Silencing of Protein Kinase C Zeta Induces Apoptosis Avoidance through ATM/Chk-2 Inactivation in Dedifferentiated Chondrosarcoma

PROVIDER: PRJNA767685 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16134574_1.fastq.gz	Fastqsanger.gz
	SRR16134574_2.fastq.gz	Fastqsanger.gz
	SRR16134575_1.fastq.gz	Fastqsanger.gz
	SRR16134575_2.fastq.gz	Fastqsanger.gz

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Methylation Mediated Silencing of Protein Kinase C Zeta Induces Apoptosis Avoidance through ATM/Chk-2 Inactivation in Dedifferentiated Chondrosarcoma

Project description:To examine methylation levels of genes, we performed whole-genome bisulfite sequence for 2 cell lines: NDCS-1, which was established from dedifferentiated chondrosarcoma and had a fast-growing phenotype, and OUMS-27, which was established from conventional chondrosarcoma and had a slow-growing phenotype.

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Methylation profiling of dedifferentiated chondrosarcoma (DDCS) samples

Project description:Genome wide DNA methylation profiling of dedifferentiated chondrosarcoma samples. Genomic DNA was extracted from formalin-fixed paraffin-embedded (FFPE) tissue after manual macrodissection to ensure at least 10% tumor content, followed by bisulfite converstion. All samples were processed on the Infinium 850k array and scanned using the Illumina iScan, according to the manufacturer's recommended protocol.

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Methylation-mediated silencing of protein kinase C zeta induces apoptosis avoidance through ATM/CHK2 inactivation in dedifferentiated chondrosarcoma.

Project description:BackgroundDedifferentiated chondrosarcoma (DDCS) is an aggressive bone tumour with a poor prognosis and no effective treatment. Because changes in DNA methylation play critical roles in DDCS, we explored the roles that DNA methylation plays in oncogenesis to potentially identify an effective epigenetic treatment.MethodsWe identified genes downregulated in DDCS vs. conventional chondrosarcoma (CCS) due to DNA methylation using in silico analysis. The results were validated in DDCS clinical samples, and the molecular functions of the genes of interest were investigated in multiple chondrosarcoma cell lines (NDCS-1, SW1353, and OUMS-27). The therapeutic effect of decitabine, a DNA methyltransferase inhibitor, was evaluated in vitro and in vivo.ResultsPRKCZ was specifically downregulated by DNA methylation in DDCS. Overexpression of PRKCZ decreased the proliferation of NDCS-1 and SW1353 cells. PRKCZ directly bound to and activated ATM, which was followed by phosphorylation of CHK2 and subsequent apoptosis. Decitabine increased PRKCZ expression through de-methylating the promoter region of PRKCZ, which activated the ATM/CHK2 pathway and inhibited cell proliferation by inducing apoptosis.ConclusionsIncreased DNA methylation and reduced expression of PRKCZ prevents apoptosis via inactivation of the ATM/CHK2 pathway in DDCS. Decitabine-induced expression of PRKCZ represents a promising therapy for DDCS.

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