Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

DNA-hypermethylated human gastric cancer circumvents apoptosis in the absence of TP53 mutation (RNA-Seq)

ABSTRACT: Comprehensive gene expression analysis by RNA-seq was performed in various cell lines after p53-MDM2 inhibitor treatment or knockdown of the target genes for novel cancer therapeutic strategies.

ORGANISM(S): Homo sapiens

PROVIDER: GSE237451 | GEO | 2025/08/13

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

DNA-hypermethylated human gastric cancer circumvents apoptosis and premature senescence in the absence of TP53 mutation

Project description:Comprehensive DNA methylation analysis in various gastric cancer cell lines with different EBV, MSI, and p53 status. Infinium HumanMethylation450 BeadChip was used to obtain DNA methylation profiles across 485,577 CpG sites.

2025-10-02 | GSE237433 | GEO

DNA-hypermethylated human gastric cancer circumvents apoptosis in the absence of TP53 mutation.

Project description:This study was designed to identify genetic mutations specific for DNA methylation epigenotypes using exome targeted sequencing combined with genome-wide DNA methylation analysis on specimens from patients with gastric cancer. Comprehensive DNA methylation profile by Infinium 450k indicated that gastric cancer was clustered into four methylation epigenotypes (MEs): extremely high-ME (E-HME), high-ME (HME), low-ME (LME), and extremely low-ME (E-LME).

2025-08-13 | GSE99111 | GEO

DNA-hypermethylated human gastric cancer circumvents apoptosis in the absence of TP53 mutation (RNA-Seq)

Project description:DNA-hypermethylated human gastric cancer circumvents apoptosis in the absence of TP53 mutation (RNA-Seq)

| PRJNA994964 | ENA

DNA-hypermethylated human gastric cancer circumvents apoptosis and premature senescence in the absence of TP53 mutation

Project description:DNA-hypermethylated human gastric cancer circumvents apoptosis and premature senescence in the absence of TP53 mutation

| PRJNA994936 | ENA

Long non-coding RNA TILR constitutively represses TP53 and apoptosis induction in lung cancer

Project description:Recent evidence suggests that non-coding RNAs play an integral regulatory role in numerous functions in lung cancer development. Here, we report identification of a novel lncRNA, herein termed TP53-inhibiting lncRNA (TILR), which plays a role as a constitutive negative regulator of p53 expression and hence its functions including activation of downstream genes such as p21 and MDM2 and induction of apoptosis. Proteomic search for TILR-associated protein revealed the association with PCBP2, and the mid-portion of TILR was required for both PCBP2 and p53 mRNA binding. In addition, depletion of PCBP2 faithfully phenocopied effects of TILR silencing. We also found that TILR suppressed p53 expression post-transcriptionally as well as via a positive feedback loop between p53 and the Fanconi anemia pathway genes. Taken together, our findings clearly demonstrate that TILR constitutively inhibits p53 expression in cooperation with PCBP2, maintaining p53 transcriptional activity at a level sufficiently low for avoidance of spurious apoptosis induction.

2022-12-19 | GSE180940 | GEO

Long non-coding RNA TILR constitutively represses TP53 and apoptosis induction in lung cancer II

2022-12-19 | GSE180944 | GEO

Trametinib + HDM201 in CRC Patients With RAS/RAF Mutant and TP53 Wild-type Advanced/Metastatic Colorectal Cancer Mutant and TP53 Wild-type

Project description:Recent preclinical studies suggest that combining MEK and MDM2 inhibition synergize to induce apoptosis in RAS/BRAF-mutant and TP53 wild-type CRC models. In vitro, in RKO cell lines (poorly differentiated colon carcinoma cell line resistant to single agent targeting MDM2 and MEK and BRAF inhibition), the MDM2 plus MEK inhibitor combination generated a synergistic increase in apoptotic index. In vivo, in mice harboring human RKO colon tumor xenografts the combination of MDM2 plus MEK inhibition elicited 93% decreases in tumor volume. This trial is to conduct a single-center, Phase 1 dose escalation study of trametinib combined with HDM201 (a HDM2 inhibitor) in patients with advanced/metastatic RAS/RAF mutant and TP53 wt CRC.

| 2287507 | ecrin-mdr-crc

Ribo-Seq experiments in HCT116 WT and TP53-/- cells upon neocarzinostatin treatment

Project description:The transcription factor p53 exerts its tumor suppressive effects through transcriptional activation of numerous target genes controlling cell cycle arrest, apoptosis, cellular senescence and DNA repair. In addition, there is evidence that p53 influences the translation of specific mRNAs, including translational attenuation of ribosomal protein synthesis and translational activation of MDM2. A challenge in the analysis of translational control is that changes in mRNA abundance exert a kinetic (passive) effect on ribosome densities. In order to separate these passive effects from active regulation of translation efficiency in response to p53 activation, we conducted a comprehensive analysis of translational regulation by comparative analysis of mRNA levels and ribosome densities upon DNA damage induced by neocarzinostatin in wild-type and TP53-/- HCT116 colorectal carcinoma cells. Thereby, we identified a specific group of mRNAs whose translation is actively up-regulated in response to p53 activation, the majority of which are transcribed from p53 target genes including MDM2, SESN1 and CDKN1A. By subsequent polysome profile analysis, we could demonstrate that a p53-dependent switch in transcript isoform expression is responsible for translational activation of SESN1, whereas translational activation of CDKN1A occurs through a trans-acting mechanism that affects multiple transcript isoforms.

2022-04-13 | GSE166783 | GEO

P409: BCL-2/BCL-XL INHIBITION INDUCES APOPTOSIS AND CIRCUMVENTS VENETOCLAX RESISTANCE IN TP53-MUTATED ACUTE MYELOID LEUKEMIA

Project description: Not available

| S-EPMC10428793 | biostudies-literature

KT-253, A Novel MDM2 Degrader and p53 Stabilizer, Has Superior Potency and Efficacy Than MDM2 Small Molecule Inhibitors

Project description:KT-253 is a potent and selective heterobifunctional MDM2 degrader with superior activity to MDM2/p53 small molecule inhibitors. RS4;11 cells treated with KT-253 indicated no off-target protein degradation. All significantly upregulated proteins are p53 and its target genes. KT-253 overcomes p53/MDM2 feedback loop. Targeted proteomics analysis of MDM2 levels in RS4;11 cells shows that KT-253 (150 nM KT-253 for 15 minutes) can achieve greater than 90% degradation of MDM2 within 1 hour posttreatment, whereas MDM2 levels continued to increase 1 hour after treatment with DS-3032 A single dose of KT-253 drives sustained tumor regression in ALL xenografts. Targeted proteomic analysis of tumors demonstrates robust degradation of MDM2 1-hour post dosing with KT-253. This is associated with activation of the p53 pathway as evidenced by a corresponding upregulation of proteomics biomarkers p53, p21, and PHLDA3.

2025-05-07 | PXD057859 | Pride

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