Similar Datasets
Project description:Targeted Protein Degradation (TPD) encompasses two approaches that generate small molecules with similar proteasome-dependent mechanisms of action: Proteolysis-Targeting Chimeras (PROTACs) and Molecular Glues (MGs). Our goal is to develop novel MG approaches that exploit the E3 ubiquitin ligase Cereblon (CRBN) to degrade key oncogenic drivers in the leading causes of childhood cancer death: acute myeloid leukemia (AML). This project will identify new vulnerabilities and compounds that degrade hitherto undruggable transcription factors in high-risk acute leukemia (AL) and medulloblastoma (MB). Based on our preliminary data, we hypothesize that these compounds target AML cells via CK1a degradation. Our aims are to understand the mechanism by which compounds SJ001041330, SJ001043149, and SJ001043301 target AML cells using TMT proteomic approach and confirm CK1a degradation by these compounds leading to AML cell death.
2023-12-01 | PXD045230 | Pride
Project description:The goal of this study is to utilize dual host-pathogen NGS to assess transcriptomic pertubations due to multiple drug compounds, and compare between compounds to identify putative mechanism of action for novel anti-Rickettsial compounds.
2022-12-27 | GSE191095 | GEO
Project description:Targeted Protein Degradation (TPD) encompasses two approaches that generate small molecules with similar proteasome-dependent mechanisms of action: Proteolysis-Targeting Chimeras (PROTACs) and Molecular Glues (MGs). Our goal is to develop novel MG approaches that exploit the E3 ubiquitin ligase Cereblon (CRBN) to degrade key oncogenic drivers in the leading causes of childhood cancer death: acute myeloid leukemia (AML). This project will identify new vulnerabilities and compounds that degrade hitherto undruggable transcription factors in high-risk acute leukemia (AL) and medulloblastoma (MB). Based on our preliminary data, we hypothesize that compound SJ001007095 targets AML cells independent of GSPT1 degradation. Our aims are to understand the mechanism by which compound SJ001007095 targets AML cells using TMT proteomic approach and identify proteins targeted by the compound SJ001007095 leading to their degradation and consequently AML cell death.
2023-12-01 | PXD045170 | Pride
Project description:In the search of new symmetrical derivatives with anticancer activity, we have looked for novel compounds able to induce a selective proapoptotic mechanism in cancer cells. The potential antitumoral activity of several quinazoline derivatives was evaluated in vitro examining their cytotoxic effects against human breast (HTB26), colon (HT29) and bladder (T24) cancer cell lines. Non-tumoral human cell lines were used to test the selectivity of the cytotoxic compounds against cancer cells. Several compounds showed selectivity for cancer cell lines; among them, 2,4-dibencilaminoquinazoline was chosen as the best candidate and its mechanism of action was studied in more detail. This compound was tested for its ability to induce caspase-3 activation and nuclear chromatin degradation in the three cancer cell lines. A time dependent evaluation of apoptosis was performed in the three cancer cell lines, including an expression microarray study at the points of caspase activation and chromatin degradation. 2,4-dibencilaminoquinazoline treatment produces few changes in the expression of genes as evaluated by using microarrays and RT-PCR assays. In conclusion, 2,4-di-p-bromofenilaminoquinazoline is a promising anticancer drug showing cytostatic and apoptotic effects mainly in a transcription independent manner. Keywords: Apoptosis induction, time course
2005-09-21 | GSE3329 | GEO
Project description:Hypnea musciformis is a red macroalga that is widely distributed in tropical and subtropical regions. It is known to contain various bioactive compounds, including sulfated polysaccharides, flavonoids, and phlorotannins. Recent studies have investigated the potential anticancer effects of extracts from Hypnea musciformis demonstrating their have cytotoxic effects on various cancer cell lines. The anticancer effects of these extracts are thought to be due to the presence of bioactive compounds, which have been shown to have antitumor and immunomodulatory effects. However, further studies are needed to fully understand the molecular mechanisms that underlie these anticancer effects and to determine their potential as therapeutic agents for cancer treatment. We have performed transcriptome and proteome analysis in liver and colon cancer human cell lines following treatment with Hypnea musciformis macroalgae extracts to characterize its anti-tumor effect in detail at the molecular level and to link transcriptome and proteome responses to the observed phenotypes in vitro. We have identified that treatment with the macroalgae extract triggers p53-mediated response at the transcriptional and protein level in liver cancer cells, in contrast to colon cancer cells in which the effects are associated with metabolic changes. Overall, the available evidence suggests that extracts from Hypnea musciformis have the potential to serve as a source of anticancer agents in liver cancer cells through the activation of a p53-mediated anti-tumor response that is linked to inhibition of cellular proliferation and induction of apoptosis.
2023-08-04 | PXD041686 | Pride
Project description:Detection of Volatile Organic Compounds (VOC) directly from tissue by headspace analysis (skin, surgery material, other tissue) and exhaled breath is feasible using affordable user-friendly novel nano-chemo sensors that can accurately be used for screening and monitoring purpose
| 2250131 | ecrin-mdr-crc
Project description:Targeted Protein Degradation (TPD) encompasses two approaches that generate small molecules with similar proteasome-dependent mechanisms of action: Proteolysis-Targeting Chimeras (PROTACs) and Molecular Glues (MGs). Our goal is to develop novel MG approaches that exploit the E3 ubiquitin ligase Cereblon (CRBN) to degrade key oncogenic drivers in the leading causes of childhood cancer death: acute myeloid leukemia (AML). This project will identify new vulnerabilities and compounds that degrade hitherto undruggable transcription factors in high-risk acute leukemia (AL) and medulloblastoma (MB). Based on our preliminary data, we hypothesize that each of these compounds (SJ001010039, SJ001010040, SJ001010041, SJ001010047, SJ001010050) degrades CK1α in this cell line and may degrade other proteins. Our aims are to confirm that CK1α is degraded by treatment with each of these compounds and to identify any additional proteins that are targeted for degradation by these compounds.
2023-12-01 | PXD045228 | Pride
Project description:KDM6B inhibition shows anticancer activity in neuroblastoma models. However, the acting mechanism of KDM6B inhibition remains poorly understood. We used microarray to detail the global programme of gene expression underlying anticancer activity of KDM6B inhibition in neuroblastoma cells.
2021-11-03 | GSE150045 | GEO
Project description:To assess the impact of the bactericidal compounds CymA and ecumicin on the mycobacterial proteome and to monitor proteome remodeling by the AAA+ ClpC1 protease machinery, we performed a LFQ proteomics analysis treating the cells at sub-bactericidal compound concentration. We identified new players of the mycobacterial ClpC1 stress response (ClpC2 and ClpC3), as novel bacterial antibiotic resistance mechanism.
2023-06-07 | PXD037232 | Pride
Project description:To assess the impact of the bactericidal compounds CymA and ecumicin on the mycobacterial proteome and to monitor proteome remodeling by the AAA+ ClpC1 protease machinery, we performed a LFQ proteomics analysis treating the cells at bactericidal compound concentration. We identified new players of the mycobacterial ClpC1 stress response (ClpC2 and ClpC3), as novel bacterial antibiotic resistance mechanism.
2023-06-07 | PXD037234 | Pride