Gene expression changes in mouse fibroblasts (3T3) after sunitinib resistance and acute and chronic withdrawal
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ABSTRACT: Transcriptome analysis was used to identify changes in mouse fibroblasts (3T3) resistant to sunitinib (SuR) and after short and long term sunitinib withdrawal in vitro (ST-W for 48 hours and LT-W for more than 2 months, respectively).
Project description:Transcriptome analysis was used to identify changes in mouse kidney cancer cells (RENCA) resistant to sunitinib (SuR) and after short and long term sunitinib withdrawal in vitro (ST-W for 48 hours and LT-W for more than 2 months, respectively).
Project description:Transcriptome analysis was used to identify changes in human breast cancer cells (LM2-4) resistant to sunitinib (SuR) and after long term sunitinib withdrawal in vitro (LT-W for more than 6 months).
Project description:Immunodeficient RAG1-/- mice bearing MDA-MB231-LUC+ tumors of 50-70 mm3 were daily administrated by gavage with vehicle (containing, 0.5% carboxymethylcellulose, 1.8 % NaCl, 0.4 % Tween-80, 0.9 %. benzyl alcohol, and ultrapure water adjusted to pH 6.0) or sunitinib (40mg/kg/day) for 30 days followed by treatment withdrawal for 3-4 weeks to allow the tumor regrowth until reaching the same volume as that of the vehicle treated group. Mice were sacrificed when tumor reached the volume of 350-400 mm3 and RNAs of two tumors from two different mice treated with sunitinib or vehicle were extracted. One color experiment with 2 experimental conditions: Sunitinib vs Vehicle (n=2), corresponding to a total of 4 samples.
Project description:Immunodeficient RAG1-/- mice bearing MDA-MB231-LUC+ tumors of 50-70 mm3 were daily administrated by gavage with vehicle (containing, 0.5% carboxymethylcellulose, 1.8 % NaCl, 0.4 % Tween-80, 0.9 %. benzyl alcohol, and ultrapure water adjusted to pH 6.0) or sunitinib (40mg/kg/day) for 30 days followed by treatment withdrawal for 3-4 weeks to allow the tumor regrowth until reaching the same volume as that of the vehicle treated group. Mice were sacrificed when tumor reached the volume of 350-400 mm3 and RNAs of two tumors from two different mice treated with sunitinib or vehicle were extracted.
Project description:To gain insights into the mechanisms of dihydroberberine, sunitinib and dihydroberberine plus sunitinib on inhibition to A549 cells, we have employed whole genome microarray expression profiling as a discovery platform to identify different genes between dihydroberberine, sunitinib and dihydroberberine plus sunitinib-treated sample and control.
Project description:To gain insights into the mechanisms of dihydroberberine, sunitinib and dihydroberberine plus sunitinib on inhibition to A549 cells, we have employed whole genome microarray expression profiling as a discovery platform to identify different genes between dihydroberberine, sunitinib and dihydroberberine plus sunitinib-treated sample and control. A549 cells were cultivated in the absence or presence of 25?mol/L dihydroberberine, 2?mol/L sunitinib, 25?mol/L dihydroberberine plus 2?mol/L sunitinib for 48 h, followed by the Agilent Whole Human Genome Oligo Microarray
Project description:In this project, we generated chronic sunitinib-treated 786-O cell, a renal cell carcinoma cell line. In order to investigate the possible effect of GPR30 agonist, G-1, on the growth-inhibtion related signaling pathways, we treated either parental both parental and chronic sunitinib-treated 786-O cells were treated either by vehicle-only (i.e. 0.1% DMSO) or 2 μM G-1 for 48 h. Therefore, there were three groups for comparison, including G-1 treatment (G-1 vs. parental), chronic sunitinib-treatment (SunR vs. parental), and G-1 treatment in SunR cells (SunR&G-1 vs. parental).