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Potent and selective PTDSS1 inhibitor targeting collateral lethality against cancer with PTDSS2 deletion [cell_RNA-seq]

ABSTRACT: To decipher the underlying mechanism governing selective growth arrest in PTDSS1-inhibited PTDSS2-depleted cancer cells, we analyzed the transcriptomic changes brought about by comparing DMSO treated and DS07551382 treated wild type or PTDSS2-depleted cells.

ORGANISM(S): Homo sapiens

PROVIDER: GSE206516 | GEO | 2022/08/31

REPOSITORIES: GEO

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Potent and selective PTDSS1 inhibitor targeting collateral lethality against cancer with PTDSS2 deletion [xeno_RNA-seq]

Project description:To decipher the underlying mechanism governing selective growth arrest in PTDSS1-inhibited PTDSS2-depleted cancer cells, we analyzed the transcriptomic changes brought about by comparing vehecle treated and DS55980254 treated PTDSS2-KO HCT116 s.c. tumors.

2022-08-31 | GSE206517 | GEO

Potent and selective PTDSS1 inhibitor targeting collateral lethality against cancer with PTDSS2 deletion

Project description:This SuperSeries is composed of the SubSeries listed below.

2022-08-31 | GSE206518 | GEO

Genomic deletion of malic enzyme 2 confers collateral lethality in pancreas cancer

Project description:Comparison of malic enzyme 3 (ME3) depleted vs non-depleted xenograft tumors. ME3 is an isoform of ME2.

2017-08-22 | GSE80411 | GEO

CPI-0610, a potent and selective BET bromodomain inhibitor optimized for clinical development

Project description:SUDHL5 cells were treated with DMSO or 2.5 μM CPI203 for 4 hours, then processed for ChIP-Seq to obtain genome-wide binding changes for BRD4 upon treatment with a BET inhibitor.

2023-01-06 | GSE71758 | GEO

Study of Potent inhibitors for CT5-3hTERT fibroblast cell line

Project description:Data independent acquisition (DIA) mass spectrometry was used to study the potent inhibitors for cancer derived fibroblast cell line, CT5-3hTERT. The fibroblast spheroids were treated with 21 different tumor inhibitors to compare their effect in proteome in comparison to treated with DMSO.

2024-08-10 | PXD050005 | Pride

Amorfrutins are selective PPARM-NM-3 agonists with potent antidiabetic properties

Project description:Faced by an alarming incidence of metabolic diseases including obesity and type 2 diabetes worldwide, there is an urgent need for effective strategies for preventing and treating these common diseases. The nuclear receptor PPARM-NM-3 (peroxisome proliferator-activated receptor gamma) plays a crucial role in metabolism. We isolated the amorfrutins from edible parts of the plants Glychyrrhiza foetida and Amorpha fruticosa, and identified these natural products as a new chemical class to treat insulin resistance and diabetes by selectively activating PPARM-NM-3. In contrast to existing synthetic PPARM-NM-3 drugs, the amorfrutins display unique properties by separating insulin sensitization from unwanted side effects. In obese mouse models, amorfrutin treatment significantly improved important metabolic and inflammatory parameters. In summary, PPARM-NM-3 activation by selective amorfrutins derived from edible biomaterial is a promising approach to combat metabolic diseases and other diseases in which PPARM-NM-3 is involved in. GSM701612-GSM701623: Male DIO C57BL/6 mice (age 18 wks), 3 groups (n=4 each after pooling of 8 samples per group). Mice were fed over 3 wks with high fat diet (HFD) without compound (vehicle), HFD with 4 mg/kg/d rosiglitazone or with 100 mg/kg/d amorfrutin 1. Liver RNA extracted. --> 4 biological replicates, vehicle vs. rosiglitazone or amorfrutin 1 GSM702299-GSM702344: Biological replicates (n = 3-4 each) of human primary adipocytes were treated with the following compounds for 24 hours. 10M-BM-5M rosiglitazone, 10M-BM-5M pioglitazone, 30M-BM-5M telmisartan, 10M-BM-5M nTZDpa, 30M-BM-5M amorfrutin 1, 30M-BM-5M amorfrutin 2, 30M-BM-5M amorfrutin 3 or 30M-BM-5M amorfrutin 4 vs. 0.1% DMSO (vehicle)

2012-05-01 | E-GEOD-28384 | biostudies-arrayexpress

Selective inhibition of CDK7 reveals the influence of CDK7 on psoriatic CD4+ T cells

Project description:Purpose: The goals of this study are to compare the differential gene of psoriatic CD4+ T cells treated with THZ1 and DMSO Methods: RNA sequencing of psoriatic CD4+ T cells which treated with THZ1 (10 nM) or DMSO

2021-04-09 | GSE171676 | GEO

A Potent and Selective Quinoxalinone-Based STK33 Inhibitor Does Not Show Synthetic Lethality in KRAS-Dependent Cells.

Project description:The KRAS oncogene is found in up to 30% of all human tumors. In 2009, RNAi experiments revealed that lowering mRNA levels of a transcript encoding the serine/threonine kinase STK33 was selectively toxic to KRAS-dependent cancer cell lines, suggesting that small-molecule inhibitors of STK33 might selectively target KRAS-dependent cancers. To test this hypothesis, we initiated a high-throughput screen using compounds in the Molecular Libraries Small Molecule Repository (MLSMR). Several hits were identified, and one of these, a quinoxalinone derivative, was optimized. Extensive SAR studies were performed and led to the chemical probe ML281 that showed low nanomolar inhibition of purified recombinant STK33 and a distinct selectivity profile as compared to other STK33 inhibitors that were reported in the course of these studies. Even at the highest concentration tested (10 μM), ML281 had no effect on the viability of KRAS-dependent cancer cells. These results are consistent with other recent reports using small-molecule STK33 inhibitors. Small molecules having different chemical structures and kinase-selectivity profiles are needed to fully understand the role of STK33 in KRAS-dependent cancers. In this regard, ML281 is a valuable addition to small-molecule probes of STK33.

| S-EPMC3523537 | biostudies-literature

Genomic deletion of malic enzyme 2 confers collateral lethality in pancreatic cancer.

Project description:The genome of pancreatic ductal adenocarcinoma (PDAC) frequently contains deletions of tumour suppressor gene loci, most notably SMAD4, which is homozygously deleted in nearly one-third of cases. As loss of neighbouring housekeeping genes can confer collateral lethality, we sought to determine whether loss of the metabolic gene malic enzyme 2 (ME2) in the SMAD4 locus would create cancer-specific metabolic vulnerability upon targeting of its paralogous isoform ME3. The mitochondrial malic enzymes (ME2 and ME3) are oxidative decarboxylases that catalyse the conversion of malate to pyruvate and are essential for NADPH regeneration and reactive oxygen species homeostasis. Here we show that ME3 depletion selectively kills ME2-null PDAC cells in a manner consistent with an essential function for ME3 in ME2-null cancer cells. Mechanistically, integrated metabolomic and molecular investigation of cells deficient in mitochondrial malic enzymes revealed diminished NADPH production and consequent high levels of reactive oxygen species. These changes activate AMP activated protein kinase (AMPK), which in turn directly suppresses sterol regulatory element-binding protein 1 (SREBP1)-directed transcription of its direct targets including the BCAT2 branched-chain amino acid transaminase 2) gene. BCAT2 catalyses the transfer of the amino group from branched-chain amino acids to ?-ketoglutarate (?-KG) thereby regenerating glutamate, which functions in part to support de novo nucleotide synthesis. Thus, mitochondrial malic enzyme deficiency, which results in impaired NADPH production, provides a prime 'collateral lethality' therapeutic strategy for the treatment of a substantial fraction of patients diagnosed with this intractable disease.

| S-EPMC5398413 | biostudies-literature

Targeting aberrant sialylation and fucosylation in prostate cancer cells using potent metabolic inhibitors

Project description:To identify signalling pathways altered by treating prostate cancer cells with the metabolic inhibitors P-SiaFNEtoc, Fucotrim I and Fucotrim II, we treated CWR22Rv1 cells with P-SiaFNEtoc, Fucotrim I and Fucotrim II for 72 hours and their respective vehicle control with DMSO. We then performed differential gene expression, Gene Ontology and GSEA analyses using data obtained from RNA-seq of the control and treated cell lines.

2023-10-27 | GSE232621 | GEO

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