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ABSTRACT: FOXM1 Cistrome Predicts Breast Cancer Metastatic Outcome Better Than FOXM1 Expression Levels or Tumor Proliferation Index

PROVIDER: PRJNA296811 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR2390493.fastq.gz	Fastqsanger.gz
	SRR2390494.fastq.gz	Fastqsanger.gz
	SRR2390495.fastq.gz	Fastqsanger.gz
	SRR2390496.fastq.gz	Fastqsanger.gz
	SRR2390497.fastq.gz	Fastqsanger.gz

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Project description:FOXM1 Cistrome Predicts Breast Cancer Metastatic Outcome Better Than FOXM1 Expression Levels or Tumor Proliferation Index [ChIP-Seq]

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Project description:FOXM1 Cistrome Predicts Breast Cancer Metastatic Outcome Better Than FOXM1 Expression Levels or Tumor Proliferation Index [RNA-Seq]

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FOXM1 Cistrome Predicts Breast Cancer Metastatic Outcome Better Than FOXM1 Expression Levels or Tumor Proliferation Index [ChIP-Seq]

Project description:FOXM1 is a key transcription factor regulating cell cycle progression, DNA damage response, and a host of other hallmark cancer features, but the role of the FOXM1 cistrome in driving estrogen receptor-positive (ER+) vs. ER- breast cancer clinical outcomes remains undefined. Chromatin immunoprecipitation sequencing (ChIP-Seq) coupled with RNA sequencing (RNA-Seq) analyses was used to identify FOXM1 target genes in breast cancer cells (MCF-7) where FOXM1 expression was either induced by cell proliferation or repressed by p53 upregulation.

2015-10-26 | E-GEOD-72977 | biostudies-arrayexpress

FOXM1 Cistrome Predicts Breast Cancer Metastatic Outcome Better Than FOXM1 Expression Levels or Tumor Proliferation Index [RNA-Seq]

2015-10-26 | E-GEOD-73370 | biostudies-arrayexpress

Coordinated Activation of c-Src and FOXM1 Drives Tumor Cell Proliferation and Breast Cancer Progression

Project description:Activation of the tyrosine kinase c-Src promotes breast cancer progression and poor outcome, yet the underlying mechanisms are incompletely understood. Here, we show that deleting c-Src abrogates the activity of Forkhead Box M1 (FOXM1), a master transcriptional regulator of the cell cycle, in a genetically engineered model mimicking the Luminal B molecular subtype of breast cancer. By phosphorylating it on two tyrosine residues, c-Src stimulates the nuclear localization of FOXM1 and the expression of its target genes, including key regulators of G2-M cell cycle progression as well as c-Src itself. This positive feedback loop drives proliferation in genetically engineered and patient-derived models of Luminal B-like breast cancer. Targeting this mechanism, including through novel compounds that destabilize the FOXM1 protein, induces G2-M cell cycle arrest and apoptosis, blocking tumor progression and impairing metastasis. We identify positive correlation of FOXM1 and c-Src expression in human breast cancer and show that the expression of FOXM1 target genes predicts poor outcome and associates with the Luminal B subtype, which responds poorly to approved therapies. These findings indicate that a regulatory network centered on c-Src and FOXM1 is a targetable vulnerability in aggressive luminal breast cancers.

2023-03-03 | GSE224876 | GEO

FOXM1 Cistrome Predicts Breast Cancer Metastatic Outcome Better Than FOXM1 Expression Levels or Tumor Proliferation Index [ChIP-Seq]

2015-10-26 | GSE72977 | GEO

FOXM1 Cistrome Predicts Breast Cancer Metastatic Outcome Better Than FOXM1 Expression Levels or Tumor Proliferation Index [RNA-Seq]

2015-10-26 | GSE73370 | GEO

Breast cancer and liver tissue biopsies used to develop and validate an index for liver contamination in metastatic breast cancer

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Identification of genes responsible for RelA-dependent proliferation arrest in HMEC conditionally expressing RelA

Project description:Immuno-histochemistry for RelA in breast tumors revealed a range of staining intensity and negative correlation between RelA levels and proliferation-index in estrogen receptor-positive tumors. Conditional expression of RelA arrested proliferation in primary mammary and fallopian tube epithelial cells. RelA dependent CDK4 downregulation was responsible for activating the G1/S checkpoint and cell cycle arrest. RelA target genes, including Interferon Response Factors (IRF), were up-regulated in the arrested cells. Among the IRFs, IRF1 expression correlates with RelA expression. Suppressing IRF1 restored CDK4 levels and rescued RelA-dependent proliferation arrest analogous to abrogating the G1/S checkpoint or restoring CDK4 levels. Apart from cyclins, regulation of CDK4 by the RelA-IRF1 transcriptional network controls proliferation of breast tumors and predicts sensitivity to a CDK4/6 inhibitor.

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Breast cancer and liver tissue biopsies used to develop and validate an index for liver contamination in metastatic breast cancer

Project description:PURPOSE: To develop an index capable of detecting and quantifying the extent of liver RNA contamination in liver biopsies of metastatic breast cancer METHODS: We developed a microarray-based gene expression liver index by comparing the expression levels of genes in liver tissue biopsies and in primary breast cancer biopsies. The predictive performance of the index was then evaluated in defined mixtures of liver and breast cancer RNA. A calibration curve was established to allow estimation of the liver RNA content in unknown metastatic breast cancer samples. A set of liver biopsies and primary breast cancer biopsies were used to identify genes that were expressed significantly higher in liver tissue. These genes were used in a liver index, which was validated in a new set of liver and primary breast cancer biopsies. A set of liver/breast cancer RNA mixtures was used to establish a calibration curve to allow quantification of liver contamination in metastatic breast cancer samples. The prediction error of the calibration curve was assessed in a new set of liver/breast cancer RNA mixtures and applied to estimate the liver content in a set of unknown metastatic breast cancer biopsies.

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