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FBXO5 degrades DOK6 to enhance cell mechanics and sensitivity to Temozolomide

ABSTRACT: FBXO5 degrades DOK6 to enhance cell mechanics and sensitivity to Temozolomide

PROVIDER: PRJNA1110241 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28995076_1.fastq.gz	Fastqsanger.gz
	SRR28995076_2.fastq.gz	Fastqsanger.gz
	SRR28995077_1.fastq.gz	Fastqsanger.gz
	SRR28995077_2.fastq.gz	Fastqsanger.gz
	SRR28995078_1.fastq.gz	Fastqsanger.gz

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FBXO5 degrades DOK6 to enhance cell mechanics and sensitivity to Temozolomide

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Project description:Temozolomide (TMZ) is a frequently used chemotherapy for glioma; however, chemoresistance is a major problem limiting its effectiveness. Thus knowledge of mechanisms underlying this outcome could improve patient prognosis. Here, we report that deletion of a regulatory element in the HOTAIR locus increases glioma cell sensitivity to TMZ and alters transcription of multiple genes. Analysis of a combination of RNA-seq, Capture HiC and patient survival data suggests that CALCOCO1 and ZC3H10 are target genes repressed by the HOTAIR regulatory element and that both function in regulating glioma cell sensitivity to TMZ. Rescue experiments and TAD analysis based on HiC data confirmed this hypothesis. We propose a new regulatory mechanism governing glioma cell TMZ sensitivity.

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| S-EPMC7229804 | biostudies-literature

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