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

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

ORGANISM(S): Homo sapiens

PROVIDER: GSE212489 | GEO | 2022/10/04

REPOSITORIES: GEO

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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 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

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

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

| PRJNA875497 | ENA

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

TRIB3 inhibition by palbociclib sensitizes prostate cancer to ferroptosis via SOX2-mediated SLC7A11 downregulation

Project description:Palbociclib is a CDK4/6 inhibitor approved for the treatment of breast cancer by suppressing cell proliferation. However, monotherapy with palbociclib was discouraging in prostate cancer, calling for a mechanism-based effective therapy. In this study, we reported in prostate cancer that palbociclib is a potent sensitizer of ferroptosis, which is worked out by downregulating the expression of TRIB3, a gene highly expressed in prostate cancer. Specifically, TRIB3 knockdown augmented the response of prostate cancer cells to ferroptosis inducers, whereas, TRIB3 overexpression rescued prostate cancer cells from palbociclib-induced ferroptosis. Mechanistically, TRIB3 inhibition by palbociclib resulted in downregulation of SOX2, which subsequently led to compromised expression of SLC7A11, a cystine/glutamate antiporter that counteracts ferroptosis. Functionally, a combined treatment of palbociclib with ferroptosis inducer significantly suppressed prostate cancer growth in a xenograft tumor model. Together, these results uncover an essential role of TRIB3/SOX2/SLC7A11 axis in palbociclib-induced ferroptosis, suggesting palbociclib a promising targeted therapy in combine with ferroptosis induction for the treatment of prostate cancer.

2024-10-31 | GSE273622 | GEO

mRNA expression of Control or TRIB3-silenced MCF7 cells

Project description:mRNA expression of Control or TRIB3-silenced MCF7 cells

| PRJNA479849 | ENA

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

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

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