Unknown,Transcriptomics,Genomics,Proteomics

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RNA-seq of mouse colon to investigate how suppression of HSF1 activity by wildtype p53 creates a driving force for p53 loss-of-heterozygosity

ABSTRACT: Mice with colonic tumors (chemically induced by AOM/DSS) were treated with Nutlin or control vehicle solution to analyze p53 target gene expression in vivo.

INSTRUMENT(S): Illumina NovaSeq 6000

ORGANISM(S): Mus musculus

SUBMITTER: Florian Wegwitz 

PROVIDER: E-MTAB-10041 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

Suppression of HSF1 activity by wildtype p53 creates a driving force for p53 loss-of-heterozygosity.

Isermann Tamara T   Şener Özge Çiçek ÖÇ   Stender Adrian A   Klemke Luisa L   Winkler Nadine N   Neesse Albrecht A   Li Jinyu J   Wegwitz Florian F   Moll Ute M UM   Schulz-Heddergott Ramona R  

Nature communications 20210629 1

The vast majority of human tumors with p53 mutations undergo loss of the remaining wildtype p53 allele (loss-of-heterozygosity, p53LOH). p53LOH has watershed significance in promoting tumor progression. However, driving forces for p53LOH are poorly understood. Here we identify the repressive WTp53-HSF1 axis as one driver of p53LOH. We find that the WTp53 allele in AOM/DSS chemically-induced colorectal tumors (CRC) of p53<sup>R248Q/+</sup> mice retains partial activity and represses heat-shock fa  ...[more]