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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

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

PROVIDER: PRJNA750415 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15278132_1.fastq.gz	Fastqsanger.gz
	SRR15278132_2.fastq.gz	Fastqsanger.gz
	SRR15278133_1.fastq.gz	Fastqsanger.gz
	SRR15278133_2.fastq.gz	Fastqsanger.gz
	SRR15278134_1.fastq.gz	Fastqsanger.gz

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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 [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 [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 [colon 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 [colon cancer]

| PRJNA750405 | 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 [breast cancer]

| PRJNA750404 | ENA

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

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

Loss-of-Function but Not Gain-of-Function Properties of Mutant TP53 Are Critical for the Proliferation, Survival, and Metastasis of a Broad Range of Cancer Cells.

Project description:Mutations in the tumor suppressor TP53 cause cancer and impart poor chemotherapeutic responses, reportedly through loss-of-function, dominant-negative effects and gain-of-function (GOF) activities. The relative contributions of these attributes is unknown. We found that removal of 12 different TP53 mutants with reported GOFs by CRISPR/Cas9 did not impact proliferation and response to chemotherapeutics of 15 human cancer cell lines and colon cancer-derived organoids in culture. Moreover, removal of mutant TP53/TRP53 did not impair growth or metastasis of human cancers in immune-deficient mice or growth of murine cancers in immune-competent mice. DepMap mining revealed that removal of 158 different TP53 mutants had no impact on the growth of 391 human cancer cell lines. In contrast, CRISPR-mediated restoration of wild-type TP53 extinguished the growth of human cancer cells in vitro. These findings demonstrate that LOF but not GOF effects of mutant TP53/TRP53 are critical to sustain expansion of many tumor types.SignificanceThis study provides evidence that removal of mutant TP53, thereby deleting its reported GOF activities, does not impact the survival, proliferation, metastasis, or chemotherapy responses of cancer cells. Thus, approaches that abrogate expression of mutant TP53 or target its reported GOF activities are unlikely to exert therapeutic impact in cancer. See related commentary by Lane, p. 211 . This article is featured in Selected Articles from This Issue, p. 201.

| S-EPMC10850947 | biostudies-literature

Gain-of-function PPM1D mutations attenuate ischemic stroke

Project description:Gain-of-function PPM1D mutations attenuate ischemic stroke

| PRJNA1252735 | ENA

Transcriptome analysis of TP53-R248L overexpressed 19NS patient-derived glioblastoma cells

Project description:This study demonstrates the role of TP53 gain-of-function (GOF) mutation on glioblastoma progression. However, little is known about the transcriptional alteration upon TP53 GOF mutation. In this study, we found that TP53 GOF mutation (R248L mutation) promotes the enrichment of multiple gene signatures related to inflammation and chemotaxis. Particularly, through in vitro and in vivo approaches, we verified that TP53 GOF mutation enhances NFKB signaling which in turn up-regulates CCL2 and TNFA. Taken together, these results suggest the function of TP53 GOF mutation driving aggressiveness of malignant brain tumor.

2019-02-26 | GSE101980 | GEO

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 perform the analysis of transcriptomes,rRegardless of the cell background, of different mutant p53s.

2016-04-27 | GSE65458 | GEO

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