{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Costa D"],"funding":["Associazione Italiana per la Ricerca sul Cancro","Italian Ministry of Health","Italian Ministry of Health Ricerca Corrente","Compagnia di San Paolo"],"pagination":["664"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9954675"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["12(4)"],"pubmed_abstract":["The p38 inhibitor SB202190 is a necessary component of the medium used for normal colorectal mucosa cultures. Sato et al. suggested that the primary activity of SB202190 may be EGFR signaling stabilization, causing an increased phosphorylation of Erk1-2 sustaining organoid proliferation. However, the growth of some colorectal cancer (CRC)-derived organoid cultures is inhibited by this molecule via an unknown mechanism. We biochemically investigated SB202190 activity on a collection of 25 primary human CRC organoids, evaluating EGFR, Akt and Erk1-2 activation using Western blot. We found that Erk1-2 phosphorylation was induced by SB202190 in 20 organoid cultures and inhibited in 5 organoid cultures. A next-generation sequencing (NGS) analysis revealed that the inhibition of p-Erk1-2 signali"],"journal":["Cells"],"pubmed_title":["SB202190 Predicts BRAF-Activating Mutations in Primary Colorectal Cancer Organoids via Erk1-2 Modulation."],"pmcid":["PMC9954675"],"funding_grant_id":["32567","5 × 1000 funds 2015 and 2016","21648"],"pubmed_authors":["Scabini S","Mastracci L","Poggi A","Coco S","Tosetti F","Benelli R","Vene R","Grillo F","Longo L","Costa D"],"additional_accession":[]},"is_claimable":false,"name":"SB202190 Predicts BRAF-Activating Mutations in Primary Colorectal Cancer Organoids via Erk1-2 Modulation.","description":"The p38 inhibitor SB202190 is a necessary component of the medium used for normal colorectal mucosa cultures. Sato et al. suggested that the primary activity of SB202190 may be EGFR signaling stabilization, causing an increased phosphorylation of Erk1-2 sustaining organoid proliferation. However, the growth of some colorectal cancer (CRC)-derived organoid cultures is inhibited by this molecule via an unknown mechanism. We biochemically investigated SB202190 activity on a collection of 25 primary human CRC organoids, evaluating EGFR, Akt and Erk1-2 activation using Western blot. We found that Erk1-2 phosphorylation was induced by SB202190 in 20 organoid cultures and inhibited in 5 organoid cultures. A next-generation sequencing (NGS) analysis revealed that the inhibition of p-Erk1-2 signali","dates":{"release":"2023-01-01T00:00:00Z","publication":"2023 Feb","modification":"2026-04-08T12:31:05.605Z","creation":"2025-04-07T03:18:54.585Z"},"accession":"S-EPMC9954675","cross_references":{"pubmed":["36831331"],"doi":["10.3390/cells12040664"]}}