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NR4A1 suppresses breast cancer growth by repressing c-Fos-mediated lipid and redox dyshomeostasis (RNA-seq)

ABSTRACT: The precise function of NR4A1 as a transcriptional regulator in cancer remains under investigation. To investive the biological functions and molecular mechanims by which NR4A1 suppresses breast cancer growth, we perform RNA sequence analysis in NR4A1-knockout and control MCF7 cell lines to identify the alterated signaling pathway and celluar possesses in breast cancer. Besides, we also performed ChIP sequences by c-Fos ChIP in in NR4A1-knockout and control MCF7 cell lines to investigate the competitive function of NR4A1 on c-Fos binding to genome.

ORGANISM(S): Homo sapiens

PROVIDER: GSE281571 | GEO | 2024/11/18

REPOSITORIES: GEO

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NR4A1 suppresses breast cancer growth by repressing c-Fos-mediated lipid and redox dyshomeostasis (ChIP-seq)

Project description:The precise function of NR4A1 as a transcriptional regulator in cancer remains under investigation. To investive the biological functions and molecular mechanims by which NR4A1 suppresses breast cancer growth, we perform RNA sequence analysis in NR4A1-knockout and control MCF7 cell lines to identify the alterated signaling pathway and celluar possesses in breast cancer. Besides, we also performed ChIP sequences by c-Fos ChIP in in NR4A1-knockout and control MCF7 cell lines to investigate the competitive function of NR4A1 on c-Fos binding to genome.

2024-11-18 | GSE281573 | GEO

NR4A1 suppresses breast cancer growth by repressing c-Fos-mediated lipid and redox dyshomeostasis (ChIP-seq)

Project description:NR4A1 suppresses breast cancer growth by repressing c-Fos-mediated lipid and redox dyshomeostasis (ChIP-seq)

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NR4A1 suppresses breast cancer growth by repressing c-Fos-mediated lipid and redox dyshomeostasis (RNA-seq)

Project description:NR4A1 suppresses breast cancer growth by repressing c-Fos-mediated lipid and redox dyshomeostasis (RNA-seq)

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NR4A1 suppresses cancer replication stress through R-loop-dependent inhibition of immediate early gene transcriptional elongation [ChIP-seq]

Project description:Deregulation of oncogenic proliferative signals triggers replication stress in cancer cells to which they must adapt. Immediate early genes (IEGs), identified by their rapid stress-induced transient bursts of expression, are critical to integrating downstream signaling pathways. In studying tumor initiation by patient-derived breast cancer cells, we observed acquisition of open chromatin domains at the genebody and 3’-UTR of IEGs, uniquely across the genome. Through in vivo and in vitro modeling, we show that the IEG and orphan nuclear receptor NR4A1 localizes across multiple IEG genebodies, where it binds to RNA Pol II, arresting transcriptional elongation and generating extensive R-loops and accessible chromatin. Acute stress promptly removes NR4A1 from IEG genebodies, triggering immediate release of their poised transcripts. In breast cancer cells, NR4A1 overexpression increases tumorigenesis; conversely, its deletion leads to uncompensated replication stress, chromosomal instability and mitotic catastrophe, driven by deregulation of its IEG target FOS. A large fraction of primary breast and other cancers exhibit open genebody chromatin at IEGs, consistent with preserved NR4A1 function. Thus, NR4A1 mediates a novel transcriptional elongation checkpoint, unique to stress-induced genes and required for their rapid bursts of expression. Cancers that have retained this mechanism in adapting to chronic replication stress may be dependent on NR4A1 for proliferation.

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NR4A1 suppresses cancer replication stress through R-loop-dependent inhibition of immediate early gene transcriptional elongation [ATAC-seq]

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NR4A1 suppresses cancer replication stress through R-loop-dependent inhibition of immediate early gene transcriptional elongation [DRIP-seq]

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NR4A1 suppresses cancer replication stress through R-loop-dependent inhibition of immediate early gene transcriptional elongation [PRO-seq]

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NR4A1 suppresses cancer replication stress through R-loop-dependent inhibition of immediate early gene transcriptional elongation [bulk RNA-seq]

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The orphan nuclear receptor NR4A1 (Nur77, TR3) regulates oxidative and endoplasmic reticulum stress in pancreatic cancer cells

Project description:NR4A1 (Nur77, TR3) is an orphan nuclear receptor that is overexpressed in pancreatic cancer cells and tumors and exhibits pro-oncogenic activity. Knockdown of NR4A1 by RNA interference (siNR4A1) in Panc1 cells and analysis of the proteome resulted in induction of several markers of endoplasmic reticulum (ER) stress including glucose-related protein 78 (GRP78), CCAAT/enhancer-binding protein-homologous protein (CHOP), activating transcription factor-3 (ATF-3) and AFT-6. These effects were accompanied by induction of apoptosis and similar results were observed after treatment of pancreatic cancer cells with the known inactivator of NR4A1, 1,1-bis(3’-indolyl)-1-(p-hydroxyphenyl)methane (DIM-C-pPhOH). Both siNR4A1 (transfected) and DIM-C-pPhOH also induced reactive oxygen species (ROS) and induction of ROS and ER stress by these agents was attenuated after cotreatment with antioxidants. Transfection of Panc1 cells with siNR4A1 follow by analysis of gene expression by arrays identified ROS metabolism genes regulated by NR4A1. Knockdown of one of these genes, thioredoxin domain containing 5 (TXNDC5) also resulted in induction of ROS and ER stress demonstrating that NR4A1 regulates levels of ER stress and ROS in pancreatic cancer cells to facilitate cell proliferation and survival. Inactivation of this receptor by siNR4A1 or DIM-C-pPhOH decreases TXNDC5 resulting in activation of ROS/ER stress and pro-apoptotic pathways and represents a novel pathway for inducing cell death in pancreatic cancer cells. Two groups of samples are included: 1. siControl; 2. siNR4A1 treatment in PAC1 cell. Transfection of Panc1 cells with siNR4A1 follow by analysis of gene expression by arrays identified ROS metabolism genes regulated by NR4A1.

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Project description:Nr4a1 deficient rats (Nr4a1-/-) were developed using the fawn hooded hypertensive rat (FHH), which provided a genetic background susceptible to kidney injury. Both groups of animals were evaluated for blood pressure, proteinuria, renal function, and whole transcriptome gene pathway changes. Gene expression profiling was performed at week 8, 16, and 24 using kidney from FHH and Nr4a1-/- rats. To identify differentially expressed gene between FHH and Nr4a1-/- two statistical methods were utilized: (1) FWER (family-wise error rate) procedure, p<0.05 and fold-change M-BM-11.2 or greater; and/or (2) Benjamani and Hochberg FDR (false discovery rate) using p<0.05, and fold-change M-BM-11.2 or greater. Two-way ANOVA using a p<0.01 or lower was performed to identify strain X time interaction effects between groups. Gene networks and functional analysis were evaluated through the use of Ingenuity Pathways Analysis . FHH and Nr4a1-/- rats were grown to 8, 16, and 24 weeks of age and kidney tissue was harvested for transcriptome analysis (n=3 replicates/ per group/ time)

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