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RNA-seq in mouse embryonic stem cells treated with or without Adriamycin

ABSTRACT: The tumor suppressor p53 is a well-recognized transcription factor that directly regulates transcriptional activation through sequence-specific DNA binding. However, whether p53 functions as a direct transcriptional repressor has long been debatable.

ORGANISM(S): Mus musculus

PROVIDER: GSE201102 | GEO | 2022/10/29

REPOSITORIES: GEO

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Sall4 guides p53-mediated enhancer interference upon DNA damage in mouse embryonic stem cells

Project description:The tumor suppressor p53 is a well-recognized transcription factor that directly regulates transcriptional activation through sequence-specific DNA binding. However, whether p53 functions as a direct transcriptional repressor has long been debatable.

2022-10-29 | GSE201103 | GEO

p53 binding in mouse embryonic stem cells untreated or treated with adriamycin

Project description:Both p53 and the Wnt signaling pathways play important roles in tumorigenesis and development. However, few studies, particularly on a genome-wide scale, have linked these two pathways. Here we show that p53 directly regulates the Wnt signaling pathway in murine embryonic stem cells (mESCs) using an integrated genome-wide approach. A chromatin-immunoprecipitation-based microarray assay (ChIP-chip) reveals that the Wnt signaling pathway is significantly over-represented in p53 bound genes. Using gene expression microarray and real-time PCR, we demonstrate that the expressions of many Wnts are robustly induced by various stresses, including DNA damage and hypoxia that activate p53. Importantly, the activation of p53 is a prerequisite for the induction of Wnts. Moreover, conditional medium (CM) collected from ultraviolet (UV)-treated mESCs contains an anti-differentiation activity, which can be lowered by either the addition of Wnt signaling inhibitors into the CM or the reduction of p53 levels in UV-treated mESCs. These results suggest that stressed mESCs utilize the p53-Wnt signaling axis to signal neighboring mESCs to delay the differentiation. Together, our results uncover a novel connection between p53 and the Wnt signaling pathways in mediating cell-to-cell communication in mESCs, and provide insights into the functions of these two pathways in tumorigenesis and development

2010-01-19 | GSE16427 | GEO

p53 is a suppressor of the carcinoma-associated transcription factor FOXQ1

Project description:FOXQ1 transcription factors is highly induced in several types of carcinomas where it promotes tumour growth and metastasis, however, the molecular mechanisms leading to FOXQ1 deregulation in cancer are incompletely understood. Here, we used a CRISPR/Cas9-based genomic locus proteomics (GLoPro) to discover transcriptional regulators of FOXQ1 and identified the tumour suppressor p53 as a transcriptional repressor of FOXQ1 expression. ChIP-qPCR as well as complementary gain and loss-of-function assays in model cell lines indicated that p53 has multiple binding sites close to the transcription start site of the FOXQ1 promoter, and that it suppresses FOXQ1 expression in various cell types. Consistently, pharmacological activation of p53 using nutlin-3 or doxorubicin reduced FOXQ1 mRNA and protein levels in colorectal cancer cell lines harboring wild type p53. In conclusion, these results suggest that mutational loss-of-function of p53, a hallmark feature of many types of cancer, de-represses FOXQ1, which accelerates tumour progression.

2024-05-13 | PXD047868 | Pride

Downregulation of LATS kinases alters p53 to promote cell migration

Project description:p53 is a pivotal tumor suppressor and a major barrier against cancer. We now report that silencing of the Hippo pathway tumor suppressors LATS1 and LATS2 in non-transformed mammary epithelial cells reduces p53 phosphorylation and increases its association with the p52 NF-κB subunit. Moreover, it partly shifts p53’s conformation and transcriptional output towards a state resembling cancer-associated p53 mutants, and endow p53 with the ability to promote cell migration. Notably, LATS1 and LATS2 are frequently downregulated in breast cancer; we propose that such downregulation might benefit cancer by converting p53 from a tumor suppressor into a tumor facilitator.

2018-10-25 | PXD003120 | Pride

RNA-seq in mouse embryonic stem cells treated with or without Adriamycin

Project description:RNA-seq in mouse embryonic stem cells treated with or without Adriamycin

| PRJNA828417 | ENA

Expression data from mouse embryonic fibroblasts (MEFs) mdmxER-Cre;C463A/WT cells, with or without 4-Hydroxytamoxifen (4OHT) treatment.

Project description:MDMX C463A mutation disrupts its binding with MDM2, and leads insufficient of MDM2 E3 ligase activity. With that, p53 degradation would be slower. In this case, p53 remaining its tumor suppressor function without transactivation. To figure out the whole map of transcripts change in MDMX C463A mutation MEFs. We used mdmxER-Cre;C463A/WTMEFs with EtOH treatment as control group, and same cells with 4OHT treatment as experimental group for gene chip analysis.

2018-01-20 | GSE109407 | GEO

Analysis of gene expression profiles in primary embryonic fibroblasts deficient for the Ing1 locus

Project description:The ING familiy of tumor suppressor proteins control several cellular functions relevant to anti-tumor protection, like cell-cycle control, apoptosis, senescence or migration. ING proteins are functionally linked to the p53 pathway, and they participate in transcriptional control via the recognition of histone marks and recruitment of protein complexes with chromatin-modifying activity to specific promoters. Here, we have investigated the global impact of ING1 in gene regulation through genome-wide analysis of expression profiles in primary embryonic fibroblasts deficient for the Ing1 locus. We find that Ing1 has a predominant role as transcriptional repressor in this setting, affecting the expression of genes involved in a variety of cellular functions. Within the subset of genes showing differential expression, we have identified DGCR8, a protein involved in the early steps of microRNA biogenesis.

2010-10-01 | GSE18519 | GEO

U2OS ad-HIC1 target identification

Project description:The tumor suppressor gene HIC1 (Hypermethylated in Cancer 1) is essential for mammalian development and is epigenetically silenced in many human tumors. Functionally, HIC1 is involved in a complex pathway regulating P53 tumor-suppression activity. HIC1 encodes a sequence-specific transcriptional repressor containing five Krüppel-like C2H2 zinc fingers but only a few genes regulated by HIC1 have been reported, including SIRT1. Keywords: Time Series Design

2007-12-13 | GSE9854 | GEO

Expression data from mammary epithelia and mammary fibroblasts from mice with and without epithelial KrasG12D and with and without stromal p53 deletion

Project description:p53 is a known tumor suppressor. We have found that stromal p53 regulates breast cancer development, the immune landscape, and survival in an oncogene specific manner when comparing the epithelial oncogenes ErbB2 and KrasG12D In this dataset, we have evaluated mammary epithelia from mice with and without epithelial KrasG12D and with and without stromal p53 deletion. We have also evaluated mammary fibroblasts from mice with and without epithelial KrasG12D and with and without stromal p53 deletion.

2022-05-01 | GSE201935 | GEO

DBC1 regulates p53 stability via inhibition of CBP-dependent p53 polyubiquitination

Project description:The control of p53 protein stability is critical to its tumor suppressor functions. The CREB Binding Protein (CBP) transcriptional coactivator co-operates with MDM2 to maintain normally low physiologic p53 levels in cells via an exclusively cytoplasmic ‘E4’ polyubiquitination activity. Utilizing mass spectrometry to identify nuclear and cytoplasmic CBP interacting proteins that regulate compartmentalized CBP E4 activity, we identified Deleted in Breast Cancer 1 (DBC1) as a stoichiometric CBP-interacting protein that negatively regulates CBP–dependent p53 polyubiquitination, stabilizes p53, and augments p53-dependent apoptosis. TCGA analysis demonstrated that solid tumors often retain wild type p53 alleles in conjunction with DBC1 loss, supporting the hypothesis that DBC1 is selected for disruption during carcinogenesis as a surrogate for p53 functional loss. As DBC1 maintains p53 stability in the nucleus where p53 exerts its tumor suppressive transcriptional function, replacement of DBC1 functionality in DBC1-deleted tumors might also enhance p53 function and chemosensitivity for therapeutic benefit.

2019-11-13 | PXD012673 | Pride

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