Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA143975 | ENA |
REPOSITORIES: ENA
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Project description:Analysis of serum starved PC-3 cells treated with CCG-1423, Latrunculin B, or the transcription elongation inhibitor DRB for 2 or 24 hours. Results provide insights to potential therapeutic approaches to cancer metastasis. Twenty one samples in triplicate were analyzed and compared to the DMSO-treated control. The primary condition tested was the effect of the Rho-transcription pathway inhibitor, CCG-1423 As a biologically related control, the actin polymerization inhibitor, Latrunculin B, that also blocks Rho-stimulated gene transcription was tested. As a control for non-specific transcription inhibition, DRB was used. All samples, 2-hr and 24-hr treated samples were compared to the 24-hr DMSO sample.
2013-05-01 | E-GEOD-30188 | biostudies-arrayexpress
Project description:Analysis of serum starved PC-3 cells treated with CCG-1423, Latrunculin B, or the transcription elongation inhibitor DRB for 2 or 24 hours. Results provide insights to potential therapeutic approaches to cancer metastasis.
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2019-07-16 | GSE134320 | GEO
Project description:The Ras/MEK/ERK pathway has been the primary focus of targeted therapies in melanoma, given that it is aberrantly activated in almost 80% of human cutaneous melanomas (~50% BRAFV600 mutations and ~30% NRAS mutations). While targeted therapies have yielded success in BRAFV600 mutant melanoma patients, such therapies have been ineffective in NRAS mutant melanomas in part due to their cytostatic effects and primary resistance in this patient population. Here, we demonstrate that increased Rho/MRTF-pathway activation correlates with high intrinsic resistance to trametinib, a MEK inhibitor, in a panel of NRAS mutant melanoma cell lines. Combination of trametinib with the Rho/MRTF-pathway inhibitor, CCG-222740, synergistically reduced cell viability in NRAS mutant melanoma cell lines in vitro. Furthermore, the combination of CCG-222740 with trametinib induced apoptosis and reduced clonogenicity in the highly trametinib-resistant SK-Mel-147 cells. These findings suggest a role of the Rho/MRTF-pathway in high intrinsic trametinib resistance to a subset of NRAS mutant melanoma cell lines and highlights the potential of concurrently targeting the Rho/MRTF-pathway and MEK in NRAS mutant melanomas.
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Project description:RNA extracted at 240min. Samples are rRNA depleted. Expression measurement of Homo sapiens genes.
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