Expression data from Control or TRIB3-silenced HCT-8 cells
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ABSTRACT:
PROVIDER: PRJNA418984 | ENA |
REPOSITORIES: ENA
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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
Project description:To determine the critical mediator of TRIB3-enhanced Wnt/beta-catenin signaling, we examined the expression profile of genes that might regulate Wnt/beta-catenin by using mRNA microarrays. Aberrant activation of Wnt/beta-catenin signaling pathway is a major reason for the tumorigenesis of Colon cancer. However, no specific drug targeting this pathway has been in the market. Surgery combined with cytotoxic drugs are still the major therapy methods toward colon cancer. These highlighted the need for therapeutics with alternative mechanisms of action. Here we report that the elevated TRIB3 expression associates positively with Wnt/beta-catenin signaling pathway. TRIB3 interacts with beta-catenin and TCF4 to enhance the associations between TCF4/beta-catenin target genes’ promoters, which upregulates the transcriptional activity of beta-catenin, thus to promote the CSC stemness and colon cancer tumorigenesis.
2020-11-17 | GSE107094 | GEO
Project description:mRNA expression of Control or TRIB3-silenced MCF7 cells
| PRJNA479849 | ENA
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
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
Project description:Expression data from control and Angpt2 silenced mouse melanoma cells
| PRJNA610074 | ENA
Project description:We report the application of single-molecule-based sequencing technology for high-throughput profiling of RNAPII with promoters in mammalian cells. We performed ChIP sequencing with antibody to total RNAPII in TRIB3-cas9 and control group. Inspection of multiple individual traces and global analyses showed that TRIB3 deletion globally reduced association of RNAPII with promoters.
2020-10-02 | GSE126743 | GEO
Project description:Gene expression data in control (shCtrl) and B55alpha-silenced (shB55a KD) HUVECs
| PRJEB38049 | ENA
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
Project description:Glutamine, the most abundant circulating amino acid, is a central metabolite critical for the survival and growth of many tumor cells. Efforts to exploit this vulnerability have met with limited success, due to the inherent adaptability of tumor cells to withstand nutrient scarcity in the tumor microenvironment. This resilience has rendered glutamine-targeting therapies ineffective in clinical trials, demanding new mechanistic insights. Here, we identify the pseudokinase TRIB3 as a key mediator of the metabolic adaptation of hepatocellular carcinoma (HCC) cells to limiting glutamine availability. TRIB3 is upregulated under glutamine deprivation in a c-Jun-dependent manner, functioning in the nucleus to safeguard DNA repair fidelity, allowing the timely resolution of DNA damage and preventing replication catastrophe. TRIB3 binds to G-quadruplex DNA (G4-DNA) structures throughout the genome, recruiting the helicase DDX5 to resolve them as a cooperative functional complex. Depleting TRIB3 or DDX5 in HCC cells leads to exaggerated G4-DNA accumulation and heightened DNA damage associated with the downregulation of DNA damage response (DDR) pathways. We illustrate this effect on homologous recombination (HR) pathway genes, finding that TRIB3-DDX5 preventing G4-DNA accumulation at the BRCA1 and RAD51AP1 promoter regions that would otherwise suppress transcription. In vivo, TRIB3 silencing suppresses HCC xenograft growth, patently increasing DNA damage and apoptosis when mice were maintained on glutamine-deficient diets. Clinically, TRIB3 is overexpressed in HCC where its elevated levels correlate with poorer patient prognosis. Together findings nominate TRIB3-DDX5-G4 axis as a therapeutically exploitable metabolic dependency in HCC and possibly other malignancies with elevated TRIB3 expression.
2026-03-13 | GSE307271 | GEO