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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Transcriptional responses of mantle cell lymphoma (MCL) lines to PKC inhibition

ABSTRACT: MCL lines (biological replicates) were treated with DMSO or 2.5uM Sotrastaurin for 3hrs This experiment is designed to see if a common set of genes is affected by Sotrastaurin (STN) treatment in STN-sensitive and STN-insensitive MCL lines. MCL cells were seeded in 6well dishes and treated for 3hrs with DMSO or 2.5uM Sotrastaurin

ORGANISM(S): Homo sapiens

SUBMITTER: Joshua Korn

PROVIDER: E-GEOD-42549 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Transcriptional responses of mantle cell lymphoma (MCL) lines to PKC inhibition

Project description:MCL lines (biological replicates) were treated with DMSO or 2.5uM Sotrastaurin for 3hrs This experiment is designed to see if a common set of genes is affected by Sotrastaurin (STN) treatment in STN-sensitive and STN-insensitive MCL lines.

2013-12-01 | GSE42549 | GEO

Transcriptional responses of mantle cell lymphoma (MCL) lines to IKKB inhibition

Project description:MCL cell lines were treated with DMSO or 5uM AFN700 for 20hrs This experiment is designed to see if NFKB-target genes are downregulated by inhibition of IKKB in MCL cell lines that are insensitive to ibrutinib (BTK inhibitor) or sotrastaurin (PKC inhibitor) MCL cells were seeded in 6well dishes and treated for 20hrs with DMSO or 5uM AFN700

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Transcriptional responses of mantle cell lymphoma (MCL) after NIK knockdown

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2013-12-01 | E-GEOD-52435 | biostudies-arrayexpress

Testing rescue of AR signaling by ectopic expression of mutant AR allele in the presence of MDV-3100

Project description:Genetically engineered LNCaPs overexpressing various AR alleles were treated with 0.1% DMSO or 10uM MDV3100 for 24h prior to collection This experiment is designed to see if expressing the F876L/T877A mutant AR can rescue AR signaling in the presence of MDV3100 Engineered lines were seeded in 6-well plates for 3d with 100ng/ml doxycycline prior to treatment with 0.1% DMSO or 10uM MDV3100 for 24h

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2014-04-15 | E-GEOD-56492 | biostudies-arrayexpress

Transcriptional responses of control and MDV3100 resistant lines to DMSO or MDV3100

Project description:LNCaP-derived MDV3100-resistant clones were treated with MDV3100 for 24h prior to collection This experiment is designed to see if MDV3100 resistant clones remain responsive to MDV3100 Control and resistant clones were seeded in 6-well plates for 3d prior to treatment with DMSO or MDV3100 for 24h

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Identification of targets regulated by HSF1 in response to HSP90 inhibitors

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Inhibiting tankyrases sensitizes KRAS mutant cancer cells to MEK inhibitors by FGFR2 feedback signaling

Project description:Tankyrases (TNKS) play roles in Wnt signaling, telomere homeostasis and mitosis, offering attractive targets for anti-cancer treatment. Using unbiased combination screening in a large panel of cancer cell lines, we have identified a strong synergy between TNKS and MEK inhibitors in KRAS mutant cancer cells. Our study uncovers a novel function of TNKS in the relief of a feedback loop induced by MEK inhibition on FGFR2 signaling pathway. Moreover, dual inhibition of TNKS and MEK leads to more robust apoptosis and anti-tumor activity both in vitro and in vivo than effects observed by previously reported MEK inhibitor combinations. Altogether, our results show how a novel combination of TNKS and MEK inhibitors can be highly effective in targeting KRAS mutant cancers by suppressing a newly discovered resistance mechanism. This experiment is designed to detect genes differentially expressed in the combination treatment compared to others SW480 cells were seeded in 10cm dishes and treated for 4h and 16h with DMSO, TNKS inhibitor (TNKSi : NVP-TNKS656), MEK inhibitor (MEKi : AZD6244) or the combination of both at 1uM final

2014-03-06 | E-GEOD-55624 | biostudies-arrayexpress

Identification of targets regulated by SELP in HSC

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2014-05-09 | E-GEOD-57459 | biostudies-arrayexpress

Isocitrata Dehydrogenase (IDH) Mutations Promote a Reversible ZEB1/mir-200-Dependent Epithelial Mesenchymal Transition (EMT)

Project description:Mutations in the genes encoding isocitrate dehydrogenase 1 and 2 (IDH1/2) occur in a variety of tumor types, resulting in production of the proposed oncometabolite, 2-hydroxyglutarate (2-HG). How mutant IDH and 2-HG alter signaling pathways to promote cancer, though, remains unclear. Additionally, there exist relatively few cell lines with IDH mutations. To examine the effect of endogenous IDH mutations and 2-HG, we created a panel of isogenic epithelial cell lines with either wild-type IDH1/2 or clinically relevant IDH1/2 mutations. Differences were noted in the ability of IDH mutations to cause robust 2-HG accumulation. IDH1/2 mutants that produce high levels of 2-HG cause an epithelial-mesenchymal transition (EMT)-like phenotype, characterized by changes in EMT-related gene expression and cellular morphology. 2-HG is sufficient to recapitulate aspects of this phenotype in the absence of an IDH mutation. In the cells types examined, mutant IDH-induced EMT is dependent on upregulation of the transcription factor ZEB1 and downregulation of the mir-200 family of microRNAs. Furthermore, sustained knockdown of IDH1 in IDH1 R132H mutant cells is sufficient to reverse many characteristics of EMT, demonstrating that continued expression of mutant IDH is required to maintain this phenotype. These results suggest mutant IDH proteins can reversibly deregulate discrete signaling pathways that contribute to tumorigenesis 9 HCT116 isogenic clones with wild-type or IDH1/2 mutations. Samples were analyzed in duplicate.

2012-10-25 | E-GEOD-41802 | biostudies-arrayexpress

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