E-PROT-23
Ontology highlight
ABSTRACT:
PROVIDER: E-PROT-23 | ExpressionAtlas | 2021-05-25
REPOSITORIES: ExpressionAtlas
Similar Datasets
Project description:Pharmacoproteomic characterisation of human colon and rectal cancer
2021-05-25 | E-PROT-24 | ExpressionAtlas
Project description:Mitogen-activated protein kinases (MEK 1/2) are central components of the RAS signaling pathway and attractive targets for cancer therapy. However, PIK3CA mutation, which commonly co-occurs with KRAS mutation, offered resistance to MEK inhibitor through activation of PI3K-AKT signaling. We identified a gene that cooperates with MEK inhibitors to forcefully treat PIK3CA mutant colon cancer cells. -catenin, a key molecule of the WNT pathway, emerged as a candidate by protein/Ab Chip array. MEK inhibitor treatment led to a decrease in -catenin in PIK3CA wild-type colon cancer cells but not in PIK3CA mutant colon cancer cells. Tumor regression was promoted by a combination of MEK inhibitor and NVP-TNS656, which targets the WNT pathway. Furthermore, combined inhibition of MEK and -catenin by NVP-TNS656 promoted tumor regression in colon cancer patient-derived xenograft (PDX) models expressing mutant PIK3CA. Taken together, we propose that inhibition of the WNT pathway, particularly -catenin, may bypass resistance to MEK inhibitor in human PIK3CA mutant colon cancer. Additionally, -catenin is a potential PD marker of MEK inhibitor resistance.
2015-08-13 | GSE71981 | GEO
Project description:Mitogen-activated protein kinases (MEK 1/2) are central components of the RAS signaling pathway and attractive targets for cancer therapy. However, PIK3CA mutation, which commonly co-occurs with KRAS mutation, offered resistance to MEK inhibitor through activation of PI3K-AKT signaling. We identified a gene that cooperates with MEK inhibitors to forcefully treat PIK3CA mutant colon cancer cells. -catenin, a key molecule of the WNT pathway, emerged as a candidate by protein/Ab Chip array. MEK inhibitor treatment led to a decrease in -catenin in PIK3CA wild-type colon cancer cells but not in PIK3CA mutant colon cancer cells. Tumor regression was promoted by a combination of MEK inhibitor and NVP-TNS656, which targets the WNT pathway. Furthermore, combined inhibition of MEK and -catenin by NVP-TNS656 promoted tumor regression in colon cancer patient-derived xenograft (PDX) models expressing mutant PIK3CA. Taken together, we propose that inhibition of the WNT pathway, particularly -catenin, may bypass resistance to MEK inhibitor in human PIK3CA mutant colon cancer. Additionally, -catenin is a potential PD marker of MEK inhibitor resistance. In the study, we identified and evaluated biomarker for response to MEK inhibitor on colon cancer cells.
2015-08-13 | E-GEOD-71981 | biostudies-arrayexpress
Project description:Comprehensive Molecular Characterization of Human Colon and Rectal Cancer
| PRJNA174201 | ENA
Project description:Characterization of the intra-tumoral heterogeneity between two iso-clonal human colon cancer sublines HCT116 and HCT116b on their ability to undergo metastatic colonization and survive under growth factor deprivation stress (GFDS). Microarray analysis revealed an upregulation of survival and metastatic genes in the highly metastatic HCT116 primary colon tumor cells compared to the poorly metastatic HCT116b primary colon tumor cells. Total RNA obtained from isolated primary colon tumors of HCT116 and HCT116b xenograft transplanted animals obtained using the orthotopic implantation of HCT116 and HCT116b human colon cancer xenografts in the cecum of male athymic BALB/c nude mice were compared at their gene expression level.
2013-02-20 | E-GEOD-44381 | biostudies-arrayexpress
Project description:Quantitative proteomics analysis of paired colorectal cancer and non-tumorigenic tissues
2023-06-21 | E-PROT-103 | ExpressionAtlas
Project description:Characterization of the intra-tumoral heterogeneity between two iso-clonal human colon cancer sublines HCT116 and HCT116b on their ability to undergo metastatic colonization and survive under growth factor deprivation stress (GFDS). Microarray analysis revealed an upregulation of survival and metastatic genes in the highly metastatic HCT116 primary colon tumor cells compared to the poorly metastatic HCT116b primary colon tumor cells.
2013-02-20 | GSE44381 | GEO
Project description:Characterization of human pineal gland proteome
2022-01-10 | E-PROT-44 | ExpressionAtlas
Project description:Here, we report the genomic-scale characterization of metastatic colon cancer transcriptome. Fresh-frozen samples was used to asses differences between normal colon, primary colon tumor an liver metastasis.
2018-09-22 | GSE89393 | GEO
Project description:Caffeic acid acetophenate exhibits anti-tumor activity. We employed proteomics to investigate the targets of caffeic acid acetophenate in human colon cancer cells. The experimental group consisted of SW480 human colon cancer cells treated with 10μM caffeic acid phenethyl for 24 hours, while the control group was treated with an equivalent volume of DMSO. Non-standard quantitative mass spectrometry was utilized to analyze differentially expressed proteins between the two groups and identify the specific target of caffeic acid acetophenate on colon cancer cells.
2023-11-01 | PXD046600 | iProX