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Only the loss-of-function but not the gain-of-function properties of mutant TP53 are critical for the sustained proliferation, survival and metastasis of a broad range of cancer cells [colon cancer]

ABSTRACT: Only the loss-of-function but not the gain-of-function properties of mutant TP53 are critical for the sustained proliferation, survival and metastasis of a broad range of cancer cells [colon cancer]

PROVIDER: PRJNA750405 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15278053_1.fastq.gz	Fastqsanger.gz
	SRR15278053_2.fastq.gz	Fastqsanger.gz
	SRR15278054_1.fastq.gz	Fastqsanger.gz
	SRR15278054_2.fastq.gz	Fastqsanger.gz
	SRR15278055_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

Only the loss-of-function but not the gain-of-function properties of mutant TP53 are critical for the sustained proliferation, survival and metastasis of a broad range of cancer cells [colon cancer]

Project description:The loss of mutant TP53 has no impact on the growth of patient derived colon cancer organoids in vivo

2023-10-13 | GSE181011 | GEO

Only the loss-of-function but not the gain-of-function properties of mutant TP53 are critical for the sustained proliferation, survival and metastasis of a broad range of cancer cells [breast cancer]

Project description:The loss of mutant TP53 did not sensitise tumour cells to chemotherapeutic agents.

2023-10-13 | GSE181010 | GEO

Only the loss-of-function but not the gain-of-function properties of mutant TP53 are critical for the sustained proliferation, survival and metastasis of a broad range of cancer cells [breast cancer]

Project description:Only the loss-of-function but not the gain-of-function properties of mutant TP53 are critical for the sustained proliferation, survival and metastasis of a broad range of cancer cells [breast cancer]

| PRJNA750404 | ENA

Only the loss-of-function but not the gain-of-function properties of mutant TP53 are critical for the sustained proliferation, survival and metastasis of a broad range of cancer cells

| PRJNA750415 | ENA

Relation between TP53 GOF mutation and Osimertinib treatment in EGFR mutant lung cancer: ChIP-seq

Project description:Background: Although TP53 gain-of-function (GOF) mutations promote cancer survival, its effect on EGFR-TKI efficacy remains unclear. We established EGFR-mutant lung cancer cell lines expressing various TP53 genotypes using CRISPR-Cas9 technology and found that TP53-GOF mutant cells develop an early resistance to EGFR-TKI osimertinib.The goal of this study is to elucidate the mechanisms underlying resistance to osimertinib treatment in TP53 GOF mutations through comprehensive gene analysis using ChIP-seq.

2024-01-22 | GSE253478 | GEO

26S proteasome is conserved, therapeutically relevant mediator of mutant p53 gain-of-function in cancer

Project description:Mutant p53 proteins, resulting form frequent TP53 tumor suppressor missense mutations, possess gain-of-function activities and are among the most widespread and robust oncoproteins in human tumors. They are potentially important but understudied therapeutic targets. No studies to date have distinguished common, therapeutically relevant mutant p53 gain-of-function effects, from effects specific to different mutant variants and cell backgrounds. Here we identify 26S proteasome machinery as the common downstream effector controlled by mutant p53s in Triple Negative Breast Cancer (TNBC - aggressive carcinomas with TP53 as the most frequently mutated locus) and conserved in other human cancers. We have identified this pathway using a combination of single-model, multi-method vertical analysis (whole cell proteome, RNA sequencing an ChIP sequencing) and multi-cell line, horizontal analysis of transcriptiomes. We found that different missense mutant p53s regardless of the cell background transcriptionaly activate whole 26S proteasome machinery. Proteasome activity is significantly increased in p53 mutant versus wild-type or knockdown/null status - in cellular and mouse models as well as in human breast tumors. Increased proteasome activity leads to inhibition of tumor suppressive pathways. The control of mutant p53 over proteasome transcription and activity results in the increased resistance to proteasome inhibitors. By combining the mutant p53 targeting agents and proteasome inhibitor we were able to overcome the “bounce-back” proteasome inhibitor resistance mechanism in mutant p53 bearing TNBC cells and xenografts in vivo.

2016-05-03 | PXD001673 | Pride

Combined TP53 and RB1 Loss Promotes Prostate Cancer Resistance to a Broad Spectrum of Cancer Therapeutics and Confers Vulnerability to Replication Stress

Project description:Prostate cancers (PC) with loss of the potent tumor suppressors TP53 and RB1 exhibit poor outcomes that include resistance to androgen receptor (AR) pathway antagonists. TP53 and RB1 also influence cell plasticity and are frequently lost in PCs with neuroendocrine (NE) differentiation. Therapeutic strategies that address these aggressive variant PCs are urgently needed. Using deep genomic profiling of 410 metastatic biopsies, we determined the relationships between combined TP53 and RB1 loss and PC phenotypes. Notably, 40% of TP53/RB1 deficient tumors were classified as AR-active adenocarcinomas indicating that NE differentiation is not an obligate consequence of TP53/RB1 inactivation. A gene expression signature reflecting TP53/RB1 loss was associated with diminished responses to AR antagonists and reduced survival. These tumors exhibit high proliferation rates and evidence of elevated DNA repair processes. While tumor cells lacking TP53/RB1 were highly resistant to all single agent therapeutics, the combination of pharmacological PARP and ATR inhibition produced significant responses, reflecting a clinically-exploitable vulnerability resulting from replication stress.

2020-06-01 | GSE147250 | GEO

Only the loss-of-function but not the gain-of-function properties of mutant TP53 are critical for the sustained proliferation, survival and metastasis of a broad range of cancer cells

Project description:This SuperSeries is composed of the SubSeries listed below.

2023-10-13 | GSE181016 | GEO

Compare proB cells from WT, Tp53-/-, Lnk-/-, Tp53-/-Lnk-/- mice and Tp53-/-Lnk-/-B-ALL

Project description:The adaptor protein LNK (SH2B3) has emerged as an important protein in regulating B cell development B cell leukemia. Loss-of-function mutations in LNK (SH2B3) are found in Philadelphia chromosomeâlike acute lymphoblastic leukemia (Ph-like ALL), but how LNK regulates normal B cell development or promotes leukemogenesis remains unclear. We found that combined loss of Lnk and tumor suppressors Tp53 in mice triggers a highly aggressive and transplantable precursor B-ALL. This study aims to investigate the molecular mechanism by which LNK regulates B-ALL development. We performed expression profiling of bone marrow proB progenitors from WT, Tp53-/-, Lnk-/- and preleukemic healthy Tp53/Lnk double knockout (DKO) mice, as well as leukemic bone marrow cells from DKO mice that have developed B-ALL. Results suggest that Tp53-/-Lnk-/- B-ALLs display similar gene expression profiles to human Ph-like B-ALLs, suggesting this model for preclinical and molecular studies. B220+CD19+CD43+AA4.1+IgM-NK1.1-Ly6c- bone marrow proB cells were double sorted from WT, Tp53-/-, Lnk-/- and preleukemic healthy Tp53/Lnk double knockout (DKO) mice, as well as leukemic bone marrow cells from DKO mice that have developed B-ALL. RNA was isolated using miRNeasy kit from QIAGEN and processed using the NuGEN Pico kit. The microarray analysis was performed at the PENN Molecular Profiling/Genomics Facility using GeneChip Mouse Gene 2.0ST array (Affymetrix).

2016-04-01 | E-GEOD-76940 | biostudies-arrayexpress

Proteasome machinery is instrumental in a common gain-of-function program of the p53 missense mutants in cancer.

Project description:Mutant p53 proteins, resulting from the missense mutations of the TP53 tumor suppressor gene, possess gain-of-function activities and are among the most robust oncoproteins in human tumors. They are potentially important therapeutic targets. No studies to date have distinguished common, therapeutically relevant mutant p53 gain-of-function effects from effects specific to different mutant variants and cell backgrounds. here we performed RNA-seq analysisin MDA-MB-231 (R280K) upon silencing TP53 or the control siRNA.

2016-04-27 | GSE68248 | GEO

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