Mek inhibition, NOS inhibition, and nNOS knockout
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ABSTRACT:
PROVIDER: PRJNA91979 | ENA |
REPOSITORIES: ENA
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Project description:embryonic cortical neuron treated with CSS, NMDA and NMDA with Mek inhibitor: replicate 1: GSM49556, GSM49557, GSM49558 replicate 2: GSM49559, GSM49560, GSM49561 nNOS KO brain cortex and wild-type littermate brain cortex: GSM49562, GSM49563 embryonic cortical neuron treated with CSS, NMDA and NMDA with NOS inhibitor: replicate 1: GSM49618, GSM49619, GSM49620 replicate 2: GSM49621, GSM49622, GSM49623
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2006-04-26 | GSE2572 | GEO
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Project description:Molecular responses to MEK inhibition in cancer cells are complex and dynamic. We performed a time-series experiment to measure global RNA expression changes following treatment with the MEK inihibor U0126 MDA-MB-231 human breast cancer cells were grown in low-serum conditions. Treatment with U0126 was initiated in the presence of EGF. RNA was harvested at multiple time points during the course of 48 hours.
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Project description:Since gastric cancer (GC) is characterized by amplifications of receptor tyrosine kinases (RTK) and KRAS, targeting the RTK/KRAS downstream pathways could contribute to broader applicability of molecular targeted therapy in GC. Here, we assembled a panel of 49 GC cell lines and screened predictors for responsiveness to RAF/MEK/ERK pathway inhibition by comparing their sensitivity to MEK inhibition with alteration status of RTK/KRAS and phosphorylation status of RTK/KRAS downstream molecules. We found that GC cells with MET amplification or KRAS mutation tend to be sensitive to MEK inhibition. Furthermore, lower phosphorylation levels of mTORC1 targets, p70S6K and 4EBP1, was also significantly associated with sensitivity to MEK inhibition. Interestingly, the sensitive cells showed reduced mTORC1 activity accompanied by decreased rate of protein synthesis after MEK inhibition, suggesting that antiproliferative effect of MEK inhibition may be exerted through inhibition of protein synthesis, which was caused by reduced mTORC1 activity. Mechanistically, expression of some mTORC1 negative regulators, such as DDIT4, FOXO3, SESN1 and TSC1, were induced by MEK inhibition in highly-sensitive cell lines and knockdown of these negative regulators partially alleviated the suppression of mTORC1 activity and antiproliferative effect of MEK inhibition. Our data suggest that a subset of GCs, which would be distinguishable according to the predictive markers we identified, may be sensitive to MEK inhibition and have implications for the strategy in clinical trial of MEK inhibitors for GC.
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