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

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

PROVIDER: PRJNA1203633 | ENA |

REPOSITORIES: ENA

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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

Blocking LAIR1 signaling in immune cells inhibits tumor development

Project description:Blocking LAIR1 signaling in immune cells inhibits tumor development

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miRNA arrays for LPS-activated Akt1+/+ and Akt1-/- macrophages

Project description:MicroRNAs regulated by lipopolysaccharide (LPS) target genes that contribute to the inflammatory phenotype. Here we showed that the protein kinase Akt1, which is activated by LPS, positively regulated miRNAs let-7e, miR-181c but negatively regulated miR-155 and miR-125b. In silico analyses and transfection studies revealed that let-7e repressed Toll-like receptor 4 (TLR4) whereas miR-155 repressed SOCS1, two proteins critical for LPS-driven TLR signalling, which regulate endotoxin sensitivity and tolerance. As a result, Akt1-/- macrophages exhibited increased responsiveness to LPS in culture and Akt1-/- mice did not develop endotoxin tolerance in vivo. Overexpression of let-7e and suppression of miR-155 in Akt1-/- macrophages restored sensitivity and tolerance to LPS in culture and in animals. These results indicate that Akt1 regulates the response of macrophages to LPS by controlling miRNA expression. The data deposited here contain the entire analysis of miRNA profile of Akt1+/+ and Akt1-/- thioglycollate elicited peritoneal macrophages following stimulation with LPS for 3 hours in culture.

2009-08-21 | GSE17421 | GEO

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

Coronary disease associated gene TCF21 inhibits smooth muscle cell differentiation by blocking the myocardin-serum response factor pathway

Project description:Coronary disease associated gene TCF21 inhibits smooth muscle cell differentiation by blocking the myocardin-serum response factor pathway

2019-12-18 | GSE124011 | GEO

miRNA arrays for LPS-activated Akt1+/+ and Akt1-/- macrophages

2009-08-21 | E-GEOD-17421 | biostudies-arrayexpress

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

Blocking IFNRA1 inhibits Multiple Myeloma-driven regulatory T-cell expansion and immunosuppression

Project description:Blocking IFNRA1 inhibits Multiple Myeloma-driven regulatory T-cell expansion and immunosuppression

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