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Status |
Public on Mar 15, 2017 |
Title |
Epithelial-to-mesenchymal transition defines feedback activation of receptor tyrosine kinase signaling induced by MEK inhibition in KRAS mutant lung cancer |
Organism |
Homo sapiens |
Experiment type |
Expression profiling by array
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Summary |
To determine the difference of gene expression profile in epithelial and mesenchymal KRAS mutant lung cancers, epithelial NCI-H358 cells were treated with TGFβ1 (4 ng/mL) or PBS for 14 days in order to induce epithelial to mesenchymal transition (EMT). Gene expression was determined in NCI-H358 cells before and after EMT induction. In addition, in order to investigate the effect of a MEK inhibitor trametinib on gene expression, mesenchymal NCI-H1792 cells were treated with 50 nM trametinib for 48 hours. Gene expression of H1792 cells for pre- and post-trametinib treatement was determined.
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Overall design |
H358 was induced EMT by treated with TGF-beta. H1792 were treated with trametinib for 48 hours. Two independent experiments were performed
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Contributor(s) |
Ebi H, Kitai H, Tomida S |
Citation(s) |
27154822 |
Submission date |
Mar 15, 2016 |
Last update date |
Oct 03, 2019 |
Contact name |
Hiromichi Ebi |
E-mail(s) |
hebi@staff.kanazawa-u.ac.jp
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Organization name |
Kanazawa University
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Department |
Institute for Frontier Science Initiative and Cancer Research Institute
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Lab |
Ebi laboratory
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Street address |
13-1 Takaramachi
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City |
Kanazawa |
State/province |
Ishikawa |
ZIP/Postal code |
920-0934 |
Country |
Japan |
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Platforms (1) |
GPL17077 |
Agilent-039494 SurePrint G3 Human GE v2 8x60K Microarray 039381 (Probe Name version) |
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Samples (8)
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Relations |
BioProject |
PRJNA315250 |