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Transcriptional profiling of p53 mutants in KP LUAD cells

ABSTRACT: Transcriptional profiling of p53 mutants in KP LUAD cells

PROVIDER: PRJNA561864 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10033900.fastq.gz	Fastqsanger.gz
	SRR10033901.fastq.gz	Fastqsanger.gz
	SRR10033902.fastq.gz	Fastqsanger.gz
	SRR10033903.fastq.gz	Fastqsanger.gz
	SRR10033904.fastq.gz	Fastqsanger.gz

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Transcriptional profiling of p53 mutants in KP LUAD cells

Project description:Transcriptional profiling of KP LUAD cells expressing a panel of p53 mutant cDNAs.

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Domain-specific p53 mutants activate EGFR by distinct mechanisms exposing tissue-independent therapeutic vulnerabilities

Project description:Mis-sense mutations affecting TP53 promote carcinogenesis both by inactivating its tumor suppressive functions, and by conferring aberrant pro-carcinogenic activities. We report here that mis-sense mutants in the p53 DNA-binding domain (DBD) and the transactivation domain (TAD) unexpectedly activate pro-carcinogenic epidermal growth factor receptor (EGFR) signaling via distinct, previously unrecognized molecular mechanisms. DBD- and TAD-specific TP53 mutants exhibited different cellular localization patterns and induced distinct gene expression profiles. Combining mass spectrometry with drug compound screens, we identified EGFR as a major signaling factor that is stabilized by TAD and DBD mutants in the cytosolic and nuclear compartments respectively, in a tissue-independent manner. Mechanistically, TAD mutants promote EGFR-mediated signaling by enhancing EGFR interaction with AKT via DDX31 in the cytosol. Conversely, DBD mutants maintain EGFR activity in the nucleus, by blocking EGFR interaction with the phosphatase SHP1, triggering upregulation of c-Myc and Cyclin D1 levels. Therapeutically, the sensitivity of DBD mutants to EGFR inhibition is enhanced by increasing the affinity of EGFR for SHP1, while that of TAD mutants can be induced by concurrent inhibition of AKT, mTOR or PI3K signaling. Thus, our findings suggest that gain-of-function, mis-sense mutations affecting two different p53 domains promote carcinogenesis by enhancing EGFR signaling via distinctive mechanisms. Our findings imply that cancer cells bearing domain-specific mutations may have distinct and exploitable therapeutic vulnerabilities.

2023-02-17 | PXD031725 | JPOST Repository

Global and p53-dependent transcriptional response of fibroblasts to Klebsiella pneumoniae

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