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

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: GSE45758 | GEO | 2013/04/04

SECONDARY ACCESSION(S): PRJNA196178

REPOSITORIES: GEO

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

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

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

2013-04-04 | GSE45757 | GEO

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

| S-ECPF-GEOD-45765 | 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

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

Inhibition of glioblastoma dispersal by the MEK inhibitor PD0325901.

Project description:BackgroundDispersal of glioblastoma (GBM) cells leads to recurrence and poor prognosis. Accordingly, molecular pathways involved in dispersal are potential therapeutic targets. The mitogen activated protein kinase/extracellular signal regulated kinase (MAPK/ERK) pathway is commonly dysregulated in GBM, and targeting this pathway with MEK inhibitors has proven effective in controlling tumor growth. Since this pathway also regulates ECM remodeling and actin organization - processes crucial to cell adhesion, substrate attachment, and cell motility - the aim of this study was to determine whether inhibiting this pathway could also impede dispersal.MethodsA variety of methods were used to quantify the effects of the MEK inhibitor, PD0325901, on potential regulators of dispersal. Cohesion, stiffness and viscosity were quantified using a method based on ellipsoid relaxation after removal of a deforming external force. Attachment strength, cell motility, spheroid dispersal velocity, and 3D growth rate were quantified using previously described methods.ResultsWe show that PD0325901 significantly increases aggregate cohesion, stiffness, and viscosity but only when tumor cells have access to high concentrations of fibronectin. Treatment also results in reorganization of actin from cortical into stress fibers, in both 2D and 3D culture. Moreover, drug treatment localized pFAK at sites of cell-substratum adhesion. Collectively, these changes resulted in increased strength of substrate attachment and decreased motility, a decrease in aggregate dispersal velocity, and in a marked decrease in growth rate of both 2D and 3D cultures.ConclusionsInhibition of the MAPK/ERK pathway by PD0325901 may be an effective therapy for reducing dispersal and growth of GBM cells.

| S-EPMC5303286 | biostudies-literature

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.

2013-04-04 | GSE45765 | GEO

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

Testing ATRA and MEK inhibitor PD0325901 effectiveness in a nude mouse model for human MPNST xenografts.

Project description:ObjectiveMalignant peripheral nerve sheath tumors (MPNST) are aggressive sarcomas characterized by high recurrence rates and early metastases. These tumors arise more frequently within neurofibromatosis type 1 (NF1) and present with resistance during standard chemotherapy leading to increased mortality and morbidity in those patients. In vitro all-trans retinoic acid (ATRA) and MEK inhibitors (MEKi) were shown to inhibit tumor proliferation, especially when applied in combination. Therefore, we established a nude mouse model to investigate if treatment of xenografts derived from NF1 associated S462 and T265 MPNST cells respond to ATRA and the MEKi PD0325901.ResultsWe demonstrated that human NF1 associated MPNST derived from S462 but not T265 cells form solid subcutaneous tumors in Foxn1 nude mice but not in Balb/c, SHO or Shorn mice. We verified a characteristic staining pattern of human MPNST xenografts by immunohistochemistry. Therapeutic effects of ATRA and/or MEKi PD0325901 on growth of S462 MPNST xenografts in Foxn1 nude mice were not demonstrated in vitro, as we did not observe significant suppression of MPNST growth compared with placebo treatment.

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Growth-inhibitory and antiangiogenic activity of the MEK inhibitor PD0325901 in malignant melanoma with or without BRAF mutations.

Project description:The Raf/MEK/ERK pathway is an important mediator of tumor cell proliferation and angiogenesis. Here, we investigated the growth-inhibitory and antiangiogenic properties of PD0325901, a novel MEK inhibitor, in human melanoma cells. PD0325901 effects were determined in a panel of melanoma cell lines with different genetic aberrations. PD0325901 markedly inhibited ERK phosphorylation and growth of both BRAF mutant and wild-type melanoma cell lines, with IC(50) in the nanomolar range even in the least responsive models. Growth inhibition was observed both in vitro and in vivo in xenograft models, regardless of BRAF mutation status, and was due to G(1)-phase cell cycle arrest and subsequent induction of apoptosis. Cell cycle (cyclin D1, c-Myc, and p27(KIP1)) and apoptosis (Bcl-2 and survivin) regulators were modulated by PD0325901 at the protein level. Gene expression profiling revealed profound modulation of several genes involved in the negative control of MAPK signaling and melanoma cell differentiation, suggesting alternative, potentially relevant mechanisms of action. Finally, PD0325901 inhibited the production of the proangiogenic factors vascular endothelial growth factor and interleukin 8 at a transcriptional level. In conclusion, PD0325901 exerts potent growth-inhibitory, proapoptotic, and antiangiogenic activity in melanoma lines, regardless of their BRAF mutation status. Deeper understanding of the molecular mechanisms of action of MEK inhibitors will likely translate into more effective treatment strategies for patients experiencing malignant melanoma.

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