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Trib3 modulates PPARg-mediated growth inhibition by interfering with the MLL complex in breast cancer cells

ABSTRACT: Trib3 modulates PPARg-mediated growth inhibition by interfering with the MLL complex in breast cancer cells

PROVIDER: PRJNA875497 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR21382400_1.fastq.gz	Fastqsanger.gz
	SRR21382400_2.fastq.gz	Fastqsanger.gz
	SRR21382401_1.fastq.gz	Fastqsanger.gz
	SRR21382401_2.fastq.gz	Fastqsanger.gz
	SRR21382402_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

Trib3 modulates PPAR-mediated growth inhibition by interfering with the MLL complex in breast cancer cells

Project description:Dysregulation of pathways due to mutations on oncogenes or tumor suppressors that leads to aberrant expression or activity of proteins is the most well understood mechanism that drives cancer initiation and progression. TRIB3, a member of the Tribbles family of pseudokinases, is often found dysregulated in cancer and has been associated with breast cancer initiation and metastasis formation. However, the underlying mechanisms by which TRIB3 contributes to these events are far from being understood. In contrast PPAR, a well-known transcription factor that belongs to the superfamily of nuclear receptors, has gained attention in recent years as drug target in breast cancer. PPAR possess anti-proliferative abilities and inducing its expression has been shown beneficial in different cancer models. In this study, we demonstrated that TRIB3 regulates PPAR expression in breast cancer cells and that TRIB3 interacts with the WRAD complex in these cells. We showed that TRIB3 expression influence H3K4me3 levels genome wide and specifically at the PPARG locus. All in all, our study situates TRIB3 as a new epigenetic regulator and represents a new line of research for the Tribbles scientific community, opening the door for future targeted therapeutic interventions for breast cancer patients

2022-10-13 | PXD036341 | Pride

Trib3 modulates PPARg-mediated growth inhibition by interfering with the MLL complex in breast cancer cells

Project description:To study the role of Trib3 in breast cancer, we performed RNAseq in Trib3-knockdown MCF7 cells compared to control cells.

2022-10-04 | GSE212489 | GEO

TRIB3 Modulates PPARγ-Mediated Growth Inhibition by Interfering with the MLL Complex in Breast Cancer Cells.

Project description:Aberrant expression or activity of proteins are amongst the best understood mechanisms that can drive cancer initiation and progression, as well as therapy resistance. TRIB3, a member of the Tribbles family of pseudokinases, is often dysregulated in cancer and has been associated with breast cancer initiation and metastasis formation. However, the underlying mechanisms by which TRIB3 contributes to these events are unclear. In this study, we demonstrate that TRIB3 regulates the expression of PPARγ, a transcription factor that has gained attention as a potential drug target in breast cancer for its antiproliferative actions. Proteomics and phosphoproteomics analyses together with classical biochemical assays indicate that TRIB3 interferes with the MLL complex and reduces MLL-mediated H3K4 trimethylation of the PPARG locus, thereby reducing PPARγ mRNA expression. Consequently, the overexpression of TRIB3 blunts the antiproliferative effect of PPARγ ligands in breast cancer cells, while reduced TRIB3 expression gives the opposite effect. In conclusion, our data implicate TRIB3 in epigenetic gene regulation and suggest that expression levels of this pseudokinase may serve as a predictor of successful experimental treatments with PPARγ ligands in breast cancer.

| S-EPMC9503934 | biostudies-literature

The effect of TRIB3 overexpression on mouse hepatocytes

Project description:To investigate the effect of TRIB3 overexpression on regulation of lipid metabolism in hepatocytes, we isolated mouse primary hepatocytes from AAV-GFP or AAV-Trib3 mice. We then performed gene expression profiling analysis using data obtained from RNA-seq of two groups of mouse primary hepatocytes from AAV-GFP or AAV-Trib3 mice.

2023-05-28 | GSE232807 | GEO

Parishin B Blocking TRIB3-AKT1 interaction inhibits Breast cancer Lung Metastasis

Project description:TRIB3 has been reported to mediate breast cancer (BC) proliferation and metastasis by interacting with AKT1, and blocking the interaction between TRIB3 and AKT1 can inhibit the progression of BC. Besides, inhibiting TRIB3 to turn “cold tumor” hot has also been proved to be an effective therapeutic strategy for BC. Thus, this study aim to find drugs that can bind to TRIB3 to inhibit BC progression, and further elucidate its mechanism.

2024-12-27 | GSE285440 | GEO

Gene expression profiling of the effect of elevated TRIB3 expression on the transcriptional response to glucose deprivation

Project description:Gene expression profiling of HEK293-derived cell lines that are stably transfected with either a tetracycline-inducible TRIB3 expression construct (TRIB3-293 cells), tetracycline-inducible ATF4 expression construct (ATF4-293 cells) or the corresponding empty vector (Vector-293 cells). Samples from tetracycline-treated and tetracycline-untreated cell cultures were collected after a 24-hour (TRIB3-293 cells, Vector-293) or 4-hour (ATF4-293) incubation in growth medium either with or without glucose.

2016-02-09 | E-MTAB-3318 | biostudies-arrayexpress

mRNA expression of Control or TRIB3-silenced MCF7 cells

Project description:Investigation of whole genome gene expression level changes in TRIB3-silenced MCF7 cells as compared to Control MCF7 cells. Analysis of activity changes of pathways for FOXO1 phosphorylation between TRIB3-silenced and Control MCF7 cells.

2019-09-25 | GSE116671 | GEO

ChIP-Seq of TRIB3 and ATF4 in HepG2 cells treated with bortezomib

Project description:The proteasome is an appealing anti-cancer drug target and the proteasome inhibitor bortezomib has been approved for the treatment of certain types of malignancies. However, the molecular mechanisms underlying cancer cell resistance to bortezomib remain poorly understood. The pseudokinase TRIB3, an inhibitor of ATF4, is expressed at a high basal level in hepatoma cells and is strongly upregulated in response to bortezomib. To map genome-wide chromatin binding loci of TRIB3 protein, we fused a Flag tag to endogenous TRIB3 in HepG2 cells and performed ChIP-Seq. The results demonstrate that TRIB3 predominantly colocalizes with ATF4 on chromatin and the proteins reside in genomic regions containing the C/EBP-ATF motif. Bortezomib treatment leads to a robust enrichment of TRIB3 binding near genes induced by bortezomib and involved in the ER stress response and cell death. Disruption of TRIB3 increases C/EBP-ATF-driven transcription, augments ER stress and cell death in cells exposed to bortezomib, while TRIB3 overexpression enhances the cell survival. Thus, TRIB3, colocalizing with ATF4 and limiting its transcriptional activity, functions as a factor increasing resistance to bortezomib, while pharmacological over-activation of eIF2alpha-ATF4 can overcome the endogenous restraint mechanisms and sensitize cells to bortezomib.

2021-05-24 | GSE166958 | GEO

Expression data from Control or TRIB3-silenced A549 cells

Project description:To determine the critical mediator of TRIB3-enhanced EGFR recycling, we examined the expression profile of genes that might regulate EGFR recycling by using mRNA microarrays. EGFR tyrosine kinase inhibitors (TKIs) confer first line therapy for patients with non-small-cell lung cancer (NSCLC). However, patients eventually develop disease progression, often driven by inevitable acquisition of EGFR TKI resistant mutations. Currently all EGFR TKIs repress NSCLC through inhibiting the kinase activity of EGFR signaling, highlighting the need for therapeutics with alternative mechanisms of action. Here we report that the elevated TRIB3 expression associates positively with EGFR stability and NSCLC progression. TRIB3 interacts with EGFR and recruits PKCα thereby enhances PKCα-induced T654 phosphorylation, which suppresses EGFR degradation and enhances membrane recycling, EGFR downstream signaling, and NSCLC stemness.

2020-06-09 | GSE103891 | GEO

Expression data from NB4 control shRNA cells and NB4 TRIB3 shRNA cells

Project description:To identify the top 20 up-regulated genes in NB4 TRIB3 shRNA cells in comparison with NB4 control shRNA cells, we examined the microarray gene expression profile of these groups above. Despite the fact that combined therapy of all-trans retinoic acid (ATRA) with arsenic trioxide (ATO) or chemotherapy dramatically improves the prognosis of patients with acute promyelocytic leukemia (APL), these regimens can cause systemic infections and secondary leukemias. Here we report that expression of the pseudokinase Tribble 3 (TRIB3) associates positively with APL progression and therapeutic resistance. The elevated TRIB3 expression promotes APL by interacting with PML-RARa and suppressing its sumoylation, ubiquitylation and degradation. This represses PML nuclear body assembly, p53-mediated senescence, cell differentiation, and supports cellular self-renewal. Genetically inhibiting Trib3 expression or disturbing the TRIB3/PML-RARa interaction produces potent therapeutic efficacy against APL and has synergic anti-APL effects when used in combination with ATRA or ATO by promoting PML-RARa degradation and PML expression. Our study provides new insight into APL pathogenesis and a new therapeutic option against APL.

2017-05-12 | GSE95637 | GEO

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