Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

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

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE124347 | GEO | 2020/12/31

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

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.

2019-12-31 | GSE124069 | GEO

Comparison of gene expression profile of naive versus arsenic trioxide resistant acute promyelocytic leukemia cell line NB4

Project description:The aim of this study was to gain insight into the potential mechanism of resistance to arsenic trioxide (ATO). The gene expression profile of naive (NB4) (Acute promyelocytic leukemia (APL) cell line and one of its in house generated ATO resistant sub clone (NB4-VM-AsR1) was done using whole genome microarray and compared to generate the differential expression profile which will give insight into the mechanisms of ATO resistance in APL. Agilent one-color experiment,Organism: Human ,Agilent Whole Genome Human 4x44k (AMADID: 014850) , Labeling kit: Agilent Quick-Amp labeling Kit (p/n5190-0442) naive versus arsenic trioxide resistant acute promyelocytic leukemia cell line NB4

2013-08-02 | E-GEOD-42031 | biostudies-arrayexpress

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.

2024-08-01 | GSE182927 | GEO

Comparison of gene expression profile of naive versus arsenic trioxide resistant acute promyelocytic leukemia cell line NB4

2013-08-02 | GSE42031 | 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.

2023-04-24 | GSE218982 | GEO

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

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

| PRJNA595114 | ENA

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

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

| PRJNA636976 | ENA

Arsenic trioxide inhibits lung metastasis of breast cancer by suppression of TP53, TGFβ and TNFα signaling pathways

Project description:Metastasis is the main cause of mortality of breast cancer. To explore the mechanisms of arsenic trioxide (ATO) in inhibition of breast cancer metastasis, ATO regulated genes in breast cancer MDA-MB-231 and LM2-4175 cells were studied. After data analysis, ATO regulated genes were involved in TP53, TGFβ and TNFα signaling pathways. Furthermore, TGFβ and TNFα activated genes in breast cancer MDA-MB-231 cells were studied.

2023-04-16 | GSE184828 | GEO

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

2022-12-12 | GSE141892 | GEO

Regulation of gene expression in chronic lymphocytic leukemia cells in response to arsenic trioxide.

Project description:Chronic lymphocytic leukemia (CLL) is characterized by the accumulation of malignant CD5+ B lymphocytes (CLL cells) in the peripheral blood, and their progressive infiltration in lymphoid organs. Despite the efforts made, CLL remains an incurable disease. It is therefore crucial to continue searching for new therapeutic agents and targets. Arsenic trioxide (ATO) induces apoptosis in all CLL cases and it could constitute an efficient therapy for this disease. We used Affimetrix microarray technology to characterize the global gene expression profile underlying CLL cell response to ATO, with the aim of identifying the ATO mechanism of action as well as new therapeutic targets in CLL.

2016-03-21 | GSE78207 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data