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Gene expression changes in human breast cancer cells (LM2-4) after sunitinib resistance and chronic withdrawal

ABSTRACT: 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).

ORGANISM(S): Homo sapiens

PROVIDER: GSE122819 | GEO | 2018/11/22

REPOSITORIES: GEO

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Gene expression changes in mouse fibroblasts (3T3) after sunitinib resistance and acute and chronic withdrawal

Project description: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).

2018-11-22 | GSE122820 | GEO

Gene expression changes in mouse kidney cancer cells (RENCA) after sunitinib resistance and acute and chronic withdrawal

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).

2018-11-22 | GSE122821 | GEO

Gene expression changes in human breast cancer cells (LM2-4) after sunitinib resistance and chronic withdrawal

Project description:Gene expression changes in human breast cancer cells (LM2-4) after sunitinib resistance and chronic withdrawal

| PRJNA506431 | ENA

Effect of Sunitinib treatment withdrawal on Immunodeficient mice bearing MDA-MB231 tumors

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.

2014-08-24 | E-GEOD-50795 | biostudies-arrayexpress

Effect of Sunitinib treatment withdrawal on Immunodeficient mice bearing MDA-MB231 tumors

2014-08-24 | GSE50795 | GEO

Gene expression changes in mouse fibroblasts (3T3) after sunitinib resistance and acute and chronic withdrawal

Project description:Gene expression changes in mouse fibroblasts (3T3) after sunitinib resistance and acute and chronic withdrawal

| PRJNA506430 | ENA

Gene expression changes in mouse kidney cancer cells (RENCA) after sunitinib resistance and acute and chronic withdrawal

Project description:Gene expression changes in mouse kidney cancer cells (RENCA) after sunitinib resistance and acute and chronic withdrawal

| PRJNA506433 | ENA

Differentially expressed genes analysis between dihydroberberine, sunitinib and dihydroberberine plus sunitinib.

2015-06-26 | GSE70282 | GEO

Differentially expressed genes analysis between dihydroberberine, sunitinib and dihydroberberine plus sunitinib.

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

2015-06-26 | E-GEOD-70282 | biostudies-arrayexpress

Transgelin contributes to a poor response of metastatic renal cell carcinoma to sunitinib treatment

Project description:Renal cell carcinoma (RCC) represents about 2-3% of all cancers with over 400,000 new cases per year. Sunitinib, a vascular endothelial growth factor tyrosine kinase receptor inhibitor, has been used mainly for first-line treatment of metastatic clear-cell RCC with good or intermediate prognosis. However, about one third of metastatic RCC patients do not respond to sunitinib, leading to disease progression. Here we aim to find and characterize proteins associated with poor sunitinib response in a pilot proteomics study. 16 RCC tumors from patients responding (8) vs. non-responding (8) to sunitinib in 3 months after treatment initiation, together with their adjacent non-cancerous tissues, were analyzed using data independent acquisition mass spectrometry. Proteomics analysis quantified 1996 protein groups (q<0.01) and revealed 27 proteins deregulated between tumors non-responding vs. responding to sunitinib, representing a pattern of deregulated proteins potentially contributing to sunitinib resistance. Gene set enrichment analysis showed up-regulation of epithelial-to-mesenchymal transition with transgelin as one of the most significantly abundant protein. Transgelin expression was silenced by CRISPR/Cas9 and RNA interference, and the cells with reduced transgelin level exhibited significantly slower proliferation. Our data indicate that transgelin is an essential protein supporting RCC cell proliferation which could contribute to intrinsic sunitinib resistance.

2021-11-03 | PXD027065 | Pride

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