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Transcriptome analysis of mutant p53 (p53-V272M, p53-R282W) rescued by arsenic trioxide (ATO)

ABSTRACT: Transcriptome analysis of mutant p53 (p53-V272M, p53-R282W) rescued by arsenic trioxide (ATO)

PROVIDER: PRJNA636976 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11915704_1.fastq.gz	Fastqsanger.gz
	SRR11915704_2.fastq.gz	Fastqsanger.gz
	SRR11915705_1.fastq.gz	Fastqsanger.gz
	SRR11915705_2.fastq.gz	Fastqsanger.gz
	SRR11915706_1.fastq.gz	Fastqsanger.gz

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Transcriptome analysis of mutant p53 rescued by arsenic trioxide (ATO)

Project description:Transcriptome analysis of mutant p53 rescued by arsenic trioxide (ATO)

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Transcriptome analysis of mutant p53 rescued by arsenic trioxide (ATO)

Project description:The goals of this study are to compare transcriptome of mutant p53 rescued by arsenic trioxide

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Transcriptome analysis of mutant p53 (p53-V272M, p53-R282W) rescued by arsenic trioxide (ATO)

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Identification of arsenic trioxide (ATO)-rescuable p53 mutations and temperature-sensitive p53 mutations in p53-null U937 cells using a patient-derived 800 p53 mutation library

Project description:Thousands of diverse p53 mutations have been identified in cancer. The leukemia-treating drug arsenic trioxide (ATO) rescues a part of p53 mutations with high potency. To repurpose ATO in personalized p53-targeted therapy, here we quantitatively determined the frequent 800 p53 mutations, covering 95.8% p53 missense-mutation cases in cancer, for their rescue potencies of cell growth inhibitory activity and mouse tumor suppressive activity by ATO. Furthermore, we determined the temperature sensitivity of 800 mutations in mammalian U937 cells and founded that ATO preferentially rescued temperature-sensitive subtype of structural p53 mutants.

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RNAseq analysis for transcriptomes of ATO+DAC treated THP-1cell lines expressing p53-R282W or p53 wild-type

Project description:To globally evaluate to what extend the p53 mutant transcription activity can be restored by arsenic trioxide (ATO) and decitabine (DAC) co-treatment, p53-null THP-1 cells introduced with p53-R282W or wild-type p53 were treated with ATO (1 μg/ml) and DAC (5 μM). mRNA was isolated and then subject to deep sequencing, using Illumina HiSeq. The sequence reads that passed quality filters were analyzed using Cutadapt.

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TP53 wild type cells are resistant to arsenic trioxide induced dynamic transcriptional changes

Project description:Previous and our results show that cells with mutant p53 are more sensitive to arsenic trioxide (ATO) induced cell growth inhibition. To explore the underling mechanisms, we conduct a detailed analysis of the globe transcriptional profiles of ATO regulated genes in breast, colon and lung cancer cells with different p53 status. We find p53 wild type cells are resistant to ATO induced globe dynamic transcriptional changes, thus resistant to ATO induced cell growth inhibition. P53 inhibitor PFTα releases p53 mediated transcriptional resistance and increases the sensitivity of ATO in p53 wild type tumor cells.

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RNAseq analysis for transcriptomes of ATO treated U937 cell lines expressing 10 type 1 p53 mutants, type-3 p53-R273H, p53 null, or p53 wild-type

Project description:To globally evaluate to what extend type-1 p53 mutant transcription activity can be restored by arsenic trioxide (ATO) (compared to wild-type p53), p53-null U937 cells introduced with 10 frequent type-1 p53, type-3 p53-R273H (negative control), empty vector or wild-type p53 were treated with or without 1 μg/mL ATO. mRNA was isolated and then subject to deep sequencing, using Illumina HiSeq. The sequence reads that passed quality filters were analyzed using Cutadapt. Results and conclusions: The type-1 p53 mutants are the major cellular targets of ATO in the current cell contexts. The expression profiles of well-established p53 targets in cells expressing wild-type p53 highly correlated with the ones in cells expressing ATO-rescued type-1 mutants, but not those in cells expressing ATO-treated R273H. In cells harboring type-1 mutants, the median expression levels of these targets were elevated by ATO to extents comparable to wild-type p53.

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Project description:To globally evaluate to what extend the p53 mutant transcription activity can be restored by arsenic trioxide (ATO), p53-null U937 cells introduced with p53-R280I or wild-type p53 were treated with or without 1 μg/mL ATO. mRNA was isolated and then subject to deep sequencing, using Illumina HiSeq. The sequence reads that passed quality filters were analyzed using Cutadapt.

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