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Expression Data from 22 human pancreatic cancer cell lines grown in triplicates +/- MEK inhibitor CI-1040

ABSTRACT: Analysis of mRNA profiles after MEK1/2 inhibition in human pancreatic cancer cell lines reveals pathways involved in drug sensitivity. We used microarrays to find gene expression patterns associated with drug response and also identified genes regulated by the MAP kinase pathway

ORGANISM(S): Homo sapiens

PROVIDER: GSE45757 | GEO | 2013/04/04

SECONDARY ACCESSION(S): PRJNA196177

REPOSITORIES: GEO

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Expression Data from 22 human pancreatic cancer cell lines grown in triplicates +/- MEK inhibitor CI-1040

Project description:Analysis of mRNA profiles after MEK1/2 inhibition in human pancreatic cancer cell lines reveals pathways involved in drug sensitivity. We used microarrays to find gene expression patterns associated with drug response and also identified genes regulated by the MAP kinase pathway 22 pancreatic cell lines were grown in culture media containing serum and either treated with vehicle control or CI-1040 for 24 hours

2013-04-04 | E-GEOD-45757 | biostudies-arrayexpress

Expression Data from 24 orthotopic tumors grown in the pancreas of mice +/- MEK inhibitor PD0325901

2013-04-04 | GSE45758 | GEO

Expression Data from 24 orthotopic tumors grown in the pancreas of mice +/- MEK inhibitor PD0325901

Project description:Analysis of mRNA profiles after MEK1/2 inhibition in human pancreatic cancer cell lines reveals pathways involved in drug sensitivity. We used microarrays to find gene expression patterns associated with drug response and also identified genes regulated by the MAP kinase pathway 6 pancreatic cell lines were injected into the pancreas of nude mice and treated either with vehicle control or PD0325901 for 12 plus 12 hours.

2013-04-04 | E-GEOD-45758 | biostudies-arrayexpress

Expression Data from 22 human pancreatic cancer cell lines grown in triplicates +/- MEK inhibitor CI-1040

Project description: Not available

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CXMS BS3 Ras/BRAF/MEK/1433 complex

Project description:RAF-family kinases are activated by recruitment to the plasma membrane by GTP-bound RAS, where they initiate signaling through the MAP kinase cascade. Here we crosslinked (BS3), digested (trypsin), and analyzed via LC-MS/MS KRAS (human, residues 1-169) bound to intact BRAF (human) in an autoinhibited state with MEK1 (human, ) and a 14-3-3 (SF9) dimer . Analysis of this KRAS/BRAF/MEK1/14-3-3 complex reveals both interprotein and intraprotein crosslinks.

2023-10-24 | PXD042584 | Pride

Expression Data from pancreatic cancer cell lines and orthotopic tumors grown with and without MEK inhibitor

Project description: Not available

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Metabolic conversion of CI-1040 turns a cellular MEK-inhibitor into an antibacterial compound.

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Multi-omics characterization of MEK inhibitor resistant pancreatic cancer based on a genetically engineered mouse model-derived in vitro system

Project description:Tumor heterogeneity and therapy resistance are hallmarks of pancreatic ductal adenocarcinoma (PDAC). Emerging evidence supports treatment-induced resistance to be a multifactorial process mediated by cellular plasticity involving epigenetic regulation. Here, we used a multi-omics approach to analyze in detail molecular mechanisms underlying MEK inhibitor (MEKi) resistance. Therefore, we characterized different cell stages (parental, MEKi resistant, reverted after different passages of drug withdrawal) in primary cell lines derived from a genetic PDAC mouse model, thereby minimizing inter-individual heterogeneity that could distort genome-wide analyses.

2024-01-26 | PXD018093 | Pride

Combined CDK inhibition overcomes MEK inhibitor resistance in plexiform neurofibroma of neurofibromatosis type I

Project description:MEK1/2 inhibitors (MEKi) have recently achieved surprising success in treating unresectable plexiform neurofibromas (PNFs). However, few studies have investigated the mechanisms of MEKi resistance in PNF patients. We determined the efficacy of 6 different MEKi for treating PNFs, explored drug resistance mechanisms and identified potential combination therapies to overcome resistance. By screening drug efficacy among 6 MEKi in human NF1-deficient PNF cell lines, TAK-733 was found reduce PNF cell viability the most. We then cultured the TAK-733 resistant cells and explored potential targets for further treatment. Both high-throughput drug screening and RNA sequencing analyses of MEKi-resistant PNF cells identified cyclin-dependent kinase inhibitors (CDKi) as potential agents for PNFs. Dinaciclib, a CDKi, showed synergistic effects on MEKi-resistant cells. Coadministration of dinaciclib and TAK-733 significantly reduced cell viability, inhibited sphere formation and colony formation. Dinaciclib did not affect MEK signaling but decreased the expression of several prosurvival proteins, including survivin and CDK1, to induce apoptosis and inhibit mitosis. TAK-733/dinaciclib combination therapy induced tumor reduction in PNF patient-derived xenografts mouse models. Therefore, the combination of MEKi and CDKi may be promising for treating inoperable PNFs, especially when drug resistance exists. Our findings provide evidence for future clinical trials with MEKi-resistant PNF patients.

2022-05-01 | GSE173577 | GEO

Multi-omics characterization of MEK inhibitor resistant pancreatic cancer based on a genetically engineered mouse model-derived in vitro system

2024-01-29 | GSE146348 | GEO

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