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Myc activation in breast cancer is due to p53-loss and sustains self-renewal of cancer stem cells (ChIP-Seq)

ABSTRACT: Purpose: discover the downstream pathways and the mechanism of target activation by the p53:Myc axis in normal mammary and cancer stem cells Methods: we performed ChIPseq experiments from NMuMG cells grown in adhesion under standard conditions Results: the p53:Myc axis orchestrates its transcriptional response in mammary-epithelial cells via a dual and overlapping mechanism: i) a tightly controlled epistasis driven by p53 and executed by Myc, and ii) a co-operative double occupancy of their downstream effectors at different regulatory regions

ORGANISM(S): Mus musculus

PROVIDER: GSE87002 | GEO | 2019/01/21

REPOSITORIES: GEO

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Myc activation in breast cancer is due to p53-loss and sustains self-renewal of cancer stem cells (RNA-Seq)

Project description:Purpose: discover the downstream pathways and the mechanism of target activation by the p53:Myc axis in normal mammary and cancer stem cells Methods: we established mammosphere culture from normal and tumoral murine mammary glands and extracted RNA for expression analysis at passage 3 of the serial replating assay Results: These data demonstrate the existence of a set of 189 p53 and Myc common targets, which are implicated in the regulation of mitosis and are up-regulated in the ErbB2-tumor mammospheres, and suggest that these genes are crucial for the regulation of CSC numbers.

2019-01-21 | GSE87003 | GEO

EPR (BC030870) ChIP-Seq analysis in NMuMG mouse mammary gland

Project description:EPR, a lncRNA present in the chromatin fraction of NMuMG cells, controls proliferation and fate determination in mammary gland cells. We wanted to define if EPR overexpression in NMuMG cells affects the landcape of two histone activation marks (H3K4me3 and H3K27ac).

2020-04-07 | GSE148182 | GEO

p53 binding during the DNA double-strand break response

Project description:We used ChIP-seq to assess where p53 binds in the human genome and how that binding changes during the DNA double-strand break response. In particular, we considered the 1-Mb-wide window centered on the MYC locus. Contrary to previous reports, we found no evidence of p53 binding at the MYC promoter. Rather, we identified three locations downstream of MYC at which p53 was bound; binding at each of these regions increased during the DNA double-strand break response.

2017-08-02 | GSE101737 | GEO

mRNA profiling of NMuMG mouse mammary epithelial cells transformed in vitro by long-term incubation in the presence of aluminium chloride vs controls incubated in parallel in the presence of the same dilution of solvent (H2O) alone. Referred to as \\"NMuMG series I\\" in the citing manuscript (Mandriota et al., submitted).

Project description:Salts of aluminium, a chemical element devoid of biological function, are added to many industrial products of frequent use because of aluminium's chemical versatility. As a result of lifetime exposure, aluminium accumulates in several organs including the mammary gland. At concentrations in the range of those measured in the breast of women living in industrialised countries, aluminium chloride transforms human and mouse mammary epithelial cells in vitro. These results challenge the safety commonly ascribed to aluminium and suggest that it could be a human carcinogen. NMuMG is a spontaneously immortalised, non tumorigenic mouse mammary epithelial cell line originally derived from NAMRU mice that, following chronic culture in the presence of aluminium - in the form of AlCl3 x 6H2O - becomes able to form tumors and metastasis in NOD-scid and nude mice. As a part of our investigations on the mechanisms by which aluminium might transform mammary epithelial cells, we analysed the mRNA profile of NMuMG cells transformed in vitro by aluminium or the corresponding untreated controls cultured in parallel by cDNA microarray. We used the Clariom S microarray from Thermofisher, that covers more than 20'000 well annotated mRNAs. The cell culture experiment analyzed in this microarray is referred to as \\"NMuMG series I\\" in the citing manuscript (Mandriota et al., submitted).

2020-11-30 | E-MTAB-9733 | biostudies-arrayexpress

mRNA profiling of NMuMG mouse mammary epithelial cells transformed in vitro by long-term incubation in the presence of aluminium chloride vs controls incubated in parallel in the presence of the same dilution of solvent (H2O) alone. Referred to as \"NMuMG series III\" in the citing manuscript (Mandriota et al., submitted).

Project description:Salts of aluminium, a chemical element devoid of biological function, are added to many industrial products of frequent use because of aluminium's chemical versatility. As a result of lifetime exposure, aluminium accumulates in several organs including the mammary gland. At concentrations in the range of those measured in the breast of women living in industrialised countries, aluminium chloride transforms human and mouse mammary epithelial cells in vitro. These results challenge the safety commonly ascribed to aluminium and suggest that it could be a human carcinogen. NMuMG is a spontaneously immortalised, non tumorigenic mouse mammary epithelial cell line originally derived from NAMRU mice that, following chronic culture in the presence of aluminium - in the form of AlCl3 x 6H2O - becomes transformed in vitro. In this specific experiment - referred to as NMuMG series III in the citing manuscript (Mandriota et al., submitted) - transformation was assessed in vitro, by the soft agar assay. As a part of our investigations on the mechanisms by which aluminium might transform mammary epithelial cells, we analysed the mRNA profile of NMuMG cells transformed in vitro by aluminium or the corresponding untreated controls cultured in parallel by cDNA microarray. We used the Clariom S microarray from Thermofisher, that covers more than 20'000 well annotated mRNAs.

2020-11-30 | E-MTAB-9735 | biostudies-arrayexpress

Expression profiling of NMuMG progression series

Project description:We have developed a progression series of increasingly metastatic cell lines generated from the normal mammary epithelial cell line, NMuMG, to distinguish between early changes in cancer initiation and metastasis-promoting alterations.

2017-06-17 | GSE94637 | GEO

Smad2/3 binding regions in NMuMG cells

Project description:Smad2/3 binding regions in mouse mammary gland epithelial cells (NMuMG) treated with TGF-beta for 1.5 h were determined by ChIP-seq to evaluate the transcriptional mechanism of TGF-beta-Smad signaling.

2019-08-29 | GSE121254 | GEO

Transcription profiling of mouse mammary epithelial cells NMuMG treatd with TGF-b1 - time series experiment

Project description:Response of mouse mammary epithelial cells NMuMG to TGF-b1 - time course experiment. Identification of novel gene targets involved in TGF-b1-driven regulation of epithelial-mesenchymal transition (EMT).

2004-10-01 | E-MEXP-139 | biostudies-arrayexpress

Analysis of the roles of AP4 and p53 downstream of c-MYC activation in breast cancer cells.

Project description:Deregulated expression of the c-MYC oncogene induces unscheduled DNA replication, DNA damage, and activation of the p53 tumor suppressor. The AP4 transcription factor is a direct c-MYC target gene involved in cell proliferation, epithelial-mesenchymal transition, and stemness, as well as suppression of DNA damage and senescence. Here, we analyzed the role of AP4 and p53 downstream of c-MYC activation using a CRISPR/Cas9-approach in MCF-7 cells.

2023-03-01 | GSE221265 | GEO

p53 activates the long noncoding RNA Pvt1b to inhibit Myc and suppress tumorigenesis

Project description:The tumor suppressor p53 transcriptionally activates target genes to suppress cellular proliferation during stress. p53 has also been implicated in the repression of the proto-oncogene Myc, but the mechanism has remained unclear. Here, we identify Pvt1b, a p53-dependent isoform of the long noncoding RNA (lncRNA) Pvt1, expressed 50 Kb downstream of Myc, which becomes induced by DNA damage or oncogenic signaling and accumulates near its site of transcription. We show that production of the Pvt1b RNA is necessary and sufficient to suppress Myc transcription in cis without altering the chromatin organization of the locus. Inhibition of Pvt1b increases Myc levels and transcriptional activity and promotes cellular proliferation. Furthermore, Pvt1b loss accelerates tumor growth, but not tumor progression, in an autochthonous mouse model of lung cancer. These findings demonstrate that Pvt1b acts at the intersection of the p53 and Myc transcriptional networks to reinforce the anti-proliferative activities of p53.

2020-01-20 | GSE142772 | GEO

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