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Decoding Trp53 regulatory program with knockout cell transcriptomic landscape analyses [stRNA-seq]

ABSTRACT: For decades, researchers have devoted great efforts to studying the tumor suppressor gene Trp53, however, our understanding of Trp53 regulation has never reached either organism-scale or single-cell resolution. Here, we performed spatial RNA analysis to confirm the Trp53 KO-induced tumor initiation states.

ORGANISM(S): Mus musculus

PROVIDER: GSE227417 | GEO | 2025/09/10

REPOSITORIES: GEO

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Decoding Trp53 regulatory program with knockout cell transcriptomic landscape analyses [scRNA-seq]

Project description:For decades, researchers have devoted great efforts to study the tumor suppressor gene Trp53, however, our understanding of Trp53 regulation has never reached either organism-scale or single-cell resolution. We constructed single-cell transcriptomic landscape covering 18 organs of Trp53-/- mice models to explore genetic network transformations in the absence of Trp53.

2025-09-10 | GSE217662 | GEO

Decoding Trp53 regulatory program with knockout cell epigenomic landscape analyses [scATAC-seq]

Project description:For decades, researchers have devoted great efforts to study the tumor suppressor gene Trp53, however, our understanding of Trp53 regulation has never reached either organism-scale or single-cell resolution. We constructed single-cell epigenomic landscape covering 17 organs of Trp53-/- mice to explore genetic network transformations in the absence of Trp53.

2025-09-10 | GSE217661 | GEO

Identification of p53 target genes in various tissues and organs using Cut&tag

Project description:For decades, researchers have devoted great efforts to study the tumor suppressor gene Trp53. However, tissue-specific Trp53 regulation still remains elusive.Here, we used Cut&tag to analyze the p53 target gene groups in 18 tissues and organs of adult mice to decipher the tissue heterogeneity of Trp53 regulation.

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Wild Type Tumor Repressor Protein 53 (TRP53) Promotes Ovarian Cancer Cell survival

Project description:Loss of Pten in the KrasG12D;Amhr2-Cre mutant mice leads to the transformation of ovarian surface epithelial (OSE) cells and rapid development of low-grade, invasive serous adenocarcinomas. Tumors occur with 100% penetrance and express elevated expression of wild type tumor repressor protein 53 (TRP53). To test the functions of TRP53 in the Pten;Kras (Trp53+) mice, we disrupted the Trp53 gene yielding Pten;Kras(Trp53-) mice. By comparing morphology and gene expression profiles in the Trp53+ and Trp53- OSE cells, we document that wild-type TRP53 acts as a major promoter of OSE cell survival and differentiation: cells lacking Trp53 are transformed yet are less adherent, migratory and invasive and exhibit a gene expression profile more like normal OSE cells. These results provide a new paradigm: wild type TRP53 does not preferentially induce apoptotic or senescent related genes in the Pten;Kras(Trp53+) cancer cells but rather increases genes regulating DNA repair, cell cycle progression and proliferation and decreases putative tumor suppressor genes. However, if TRP53 activity is forced higher by exposure to nutlin-3a (an MDM2 antagonist), TRP53 suppresses DNA repair genes and induces the expression of genes that control cell cycle arrest and apoptosis. Thus, in the Pten;Kras(Trp53+) mutant mouse OSE cells and likely in human TP53+ low grade ovarian cancer cells, wild type TRP53 controls global molecular changes that are dependent on its activation status. These results suggest that activation of TP53 may provide a promising new therapy for managing type I ovarian cancer and other cancers in humans where wild-type TP53 is expressed. A direct comparison of ovarian surface epithelia cells from three different genotype mice

2012-06-20 | E-GEOD-34882 | biostudies-arrayexpress

Decoding Trp53 regulatory program in various tissues and organs

Project description:Decoding Trp53 regulatory program in various tissues and organs

| PRJNA899903 | ENA

Wild Type Tumor Repressor Protein 53 (TRP53) Promotes Ovarian Cancer Cell survival

2012-06-21 | GSE34882 | GEO

NRF2 activation in TRP53:P16 deficient mice drives oral squamous cell carcinoma

Project description:NRF2 activation in TRP53:P16 deficient mice drives oral squamous cell carcinoma

2024-01-31 | PXD048887 | Pride

RNAi off-target analysis in Trp53-/- mouse embryonic fibroblasts transduced with miRNA-based shRNAs targeting Trp53.

Project description:We analyzed miRNA-based shRNA off-target effects by transducing Trp53-/- MEFs at single- and high-copy with six well-characterized, potent and weak Trp53 shRNAs. To advance RNAi therapy for KRAS-mutant cancer, we developed a functionally validated library of siRNAs against RAS pathway genes that minimize off-target effects and enable combination gene silencing at low dose. We developed an in vivo model for real-time tracking of nanoparticle-based siRNA delivery and offer proof-of-principle that siRNA-mediated inhibition of a single gene (KRAS) or combinations of genes (A/B/C-RAF or KRAS+PIK3C-A/B) can impair the growth of KRAS-mutant colorectal cancer xenografts. Trp53-/- MEFs were transduced with LMP expressing Trp53 shRNAs at single copy (11-21% infection efficiency) and high copy (>98% infection efficiency), selected on puromycin and grown in absence of the selection agent before harvest. Uninfected Trp53-/- MEFs and Trp53-/- MEFs infected with an empty vector control served as M-bM-^@M-^\no shRNAM-bM-^@M-^] reference.

2014-08-01 | E-GEOD-59952 | biostudies-arrayexpress

Transcription profiling of wild type, Trp53-null and Trp53-515C/515C (encoding p53R172P) mouse embryo fibroblasts treated with gamma-radiation

Project description:Trp53-null, Trp53-515C/515C (encoding p53R172P), or wild-type mouse embryo fibroblasts were treated with 6 Gy gamma-radiation and harvested 6 hours later to compare expression profiles of genes regulated by wild-type p53 and p53R172P. Trp53-null cells were included as a negative control.

2006-11-20 | E-MEXP-917 | biostudies-arrayexpress

Ablation of Cdh1 and Trp53 in the uterus reveals novel mechanisms controlling tumor microenvironment in endometrial cancer.

Project description:Because TP53 mutation and CDH1 inactivation are the most common abnormalities found in human type II endometrial carcinomas, the contribution of dysfunctional TRP53 and CDH1 in the tumor microenvironment to induce type II endometrial cancer was characterized using mouse as a model. The results of our analysis revealed that conditional deletion of Cdh1 and Trp53 in the uterus regulated most of the genes categorized by their involvement in inflammatory responses, immune cell trafficking, cellular movement, cell-to-cell signaling and interaction and cellular growth and proliferation. A direct comparison of mouse uteri (n=3) from control, single ablation of Cdh1 or Trp53, and ablation of both Cdh1 and Trp53 at 2 months of age.

2014-06-23 | E-GEOD-48131 | biostudies-arrayexpress

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