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

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE45765 | GEO | 2013/04/04

SECONDARY ACCESSION(S): PRJNA196231

REPOSITORIES: GEO

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

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

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

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2013-04-04 | E-GEOD-45765 | biostudies-arrayexpress

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.

| S-ECPF-GEOD-45758 | biostudies-other

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

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

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

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

2013-04-04 | GSE45757 | GEO

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

MEK inhibitors cobimetinib and trametinib, regressed a gemcitabine-resistant pancreatic-cancer patient-derived orthotopic xenograft (PDOX).

Project description:A pancreatic ductal adenocarcinoma (PDAC), obtained from a patient, was grown orthotopically in the pancreatic tail of nude mice to establish a patient-derived orthotopic (PDOX) model. Seven weeks after implantation, PDOX nude mice were divided into the following groups: untreated control (n = 7); gemcitabine (100 mg/kg, i.p., once a week for 2 weeks, n = 7); cobimetinib (5 mg/kg, p.o., 14 consecutive days, n = 7); trametinib (0.3 mg/kg, p.o., 14 consecutive days, n = 7); trabectedin (0.15 mg/kg, i.v., once a week for 2 weeks, n = 7); temozolomide (25 mg/kg, p.o., 14 consecutive days, n = 7); carfilzomib (2 mg/kg, i.v., twice a week for 2 weeks, n = 7); bortezomib (1 mg/kg, i.v., twice a week for 2 weeks, n = 7); MK-1775 (20 mg/kg, p.o., 14 consecutive days, n = 7); BEZ-235 (45 mg/kg, p.o., 14 consecutive days, n = 7); vorinostat (50 mg/kg, i.p., 14 consecutive days, n = 7). Only the MEK inhibitors, cobimetinib and trametinib, regressed tumor growth, and they were more significantly effective than other therapies (p < 0.0001, respectively), thereby demonstrating the precision of the PDOX models of PDAC and its potential for individualizing pancreatic-cancer therapy.

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Identification of a new class of MDM2 inhibitor that inhibits growth of orthotopic pancreatic tumors in mice.

Project description:Background & aimsThe oncogene MDM2, which encodes an E3 ubiquitin ligase, is overexpressed in pancreatic cancers and is therefore a therapeutic target. Current inhibitors of MDM2 target the interaction between MDM2 and P53; these would have no effect on cancer cells that do not express full-length P53, including many pancreatic cancer cells. We searched for a compound that specifically inhibits MDM2 itself.MethodsWe performed a virtual screen and structure-based design to identify specific inhibitors of MDM2. We tested the activities of compounds identified on viability, proliferation, and protein levels of HPAC, Panc-1, AsPC-1, and Mia-Paca-2 pancreatic cancer cell lines. We tested whether intraperitoneal injections of one of the compounds identified affected growth of xenograft tumors from Panc-1 cells, or orthotopic tumors from Panc-1 and AsPC-1 cells (injected into pancreata), in nude mice.ResultsWe identified a compound, called SP141, which bound directly to MDM2, promoting its auto-ubiquitination and degradation by the proteasome. The compound reduced levels of MDM2 in pancreatic cancer cell lines, as well as their proliferation, with 50% inhibitory concentrations <0.5 μM (0.38-0.50 μM). Increasing concentrations of SP141 induced increasing levels of apoptosis and G2-M-phase arrest of pancreatic cancer cell lines, whether or not they expressed functional P53. Injection of nude mice with SP141 (40 mg/kg/d) inhibited growth of xenograft tumors (by 75% compared with control mice), and led to regression of orthotopic tumors.ConclusionsIn a screen for specific inhibitors of MDM2, we identified a compound called SP141 that reduces levels of MDM2 in pancreatic cancer cell lines, as well as their proliferation and ability to form tumors in nude mice. SP141 is a new class of MDM2 inhibitor that promotes MDM2 auto-ubiquitination and degradation. It might be further developed as a therapeutic agent for pancreatic cancer.

| S-EPMC4170027 | biostudies-literature

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