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Single-Cell RNA-Sequencing facilitates the effectiveness analysis of clinical-dose arsenic trioxide (ATO) treatment in reactivating V272M in AML patient and in primary AML PBMCs

ABSTRACT: The goals of this study is to reveal the transcriptome of p53-V272M rescued by ATO in AML patient and in primary AML PBMCs

ORGANISM(S): Homo sapiens

PROVIDER: GSE182926 | GEO | 2024/08/01

REPOSITORIES: GEO

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Single-Cell RNA-Sequencing facilitates the effectiveness analysis of clinical-dose arsenic trioxide (ATO) treatment in reactivating V272M in AML patient and in primary AML PBMCs

Project description:Single-Cell RNA-Sequencing facilitates the effectiveness analysis of clinical-dose arsenic trioxide (ATO) treatment in reactivating V272M in AML patient and in primary AML PBMCs

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Human HL-60 Cells: all-trans retinoic acid (ATRA) vs. ATRA plus arsenic trioxide (ATO)

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Single-Cell RNA-Sequencing facilitates the effectiveness analysis of ATO and DAC co-treatment in PBMCs from PANDA-T0 trial

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Human HL-60 Cells: all-trans retinoic acid (ATRA) vs. ATRA plus arsenic trioxide (ATO)

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Elevated Levels of Arsenic Trioxide Promote Divergent SUMOylation

Project description:ATO is a therapeutic agents used to treat APL, a disease caused by a chromosomal translocation of the RARα gene that can occur reciprocally with the PML gene. The mechanisms through which ATO function and how increased levels of ATO adversely affect the cell are not fully characterized though they involve the SUMOylation, the ubiquitylation and the degradation of the PML/RARα oncoprotein through the PML moiety. Changes in protein SUMOylation, phosphorylation and ubiquitylation were profiled using large-scale proteomic workflows on HEK293 cells following exposure to typical (1 μM) or elevated (10 μM) ATO for 4h to understand the mechanism that underlies the cytotoxicity induced with important ATO levels. Our analyses revealed that 88 proteins displayed divergent SUMOylation with elevated ATO compared to the lower dose, where the latter caused changes in SUMOylation of 4 proteins, including PML. Some of these differing SUMOylation events occurred on known substrates of caspase-3. A similar phenomenon was observed in the phosphoproteomic studies, where 48 proteins were specifically regulated with elevated ATO levels, while low ATO doses barely altered the phosphoproteome. Elevated levels of ATO cause the erroneous SUMOylation and phosphorylation of a vast amount of substrates, which may be responsible for its cytotoxic effects.

2020-04-06 | PXD016166 | Pride

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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BRD4 inhibitor JQ1 increase the sensitivity of arsenic trioxide in pancreatic cancer

Project description:Pancreatic cancer is a deadliest type of malignancy, largely due to lack of effective intervention. We here report a pair of agents, ATO and JQ1, which synergistically induce apoptosis in the malignancy. Through global and molecular approaches, we have provided evidence that these agents are both able to modulate ER stress and autophagy in the cancer, probably acting in different ways. Cross-talks between ER stress and autophagy are implicated during ATO/ATO plus JQ1 induced apoptosis, in which NRF2 appears to play a central role. 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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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.

2020-12-31 | GSE124347 | GEO

The genomic landscape of sensitivity to Arsenic Trioxide characterized by Genome-wide CRISPR-Cas9 screening

Project description:The key modifiers of sensitivity to Arsenic Trioxide (ATO) remained unclear, and we presented a genome-wide scale loss-of-function screening to identify the modulators of cell response to ATO.

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