{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Khandakar GI"],"funding":["Ministry of Education, Culture, Sports, Science and Technology","Japan Society for the Promotion of Science"],"pagination":["702"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC8869916"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["11(4)"],"pubmed_abstract":["The mitogen-activated protein kinase (MAPK)/ERK and phosphatidylinositol-3 kinase (PI3K)/AKT pathways are dysregulated in various human cancers, including pancreatic ductal adenocarcinoma (PDAC), which has a very poor prognosis due to its lack of efficient therapies. We have previously identified ACAGT-007a (GT-7), an anti-cancer compound that kills ERK-active melanoma cells by inducing ERK-dependent apoptosis. Here, we investigated the apoptosis-inducing effect of GT-7 on three PDAC cell lines and its relevance with the MAPK/ERK and PI3K/AKT signaling pathways. GT-7 induced apoptosis in PDAC cells with different KRAS mutations (MIA-Pa-Ca-2 (KRAS G12C), T3M4 (KRAS Q61H), and PANC-1 (KRAS G12D)), being T3M4 most susceptible, followed by MIA-Pa-Ca-2, and PANC-1 was most resistant to apoptosi"],"journal":["Cells"],"pubmed_title":["ACAGT-007a, an ERK MAPK Signaling Modulator, in Combination with AKT Signaling Inhibition Induces Apoptosis in KRAS Mutant Pancreatic Cancer T3M4 and MIA-Pa-Ca-2 Cells."],"pmcid":["PMC8869916"],"funding_grant_id":["JPS1411037","JP19H03376","JP20K06494"],"pubmed_authors":["Satoh R","Fujitani K","Tanabe G","Nishio K","Takasaki T","Sakai K","Sugiura R","Khandakar GI"],"additional_accession":[]},"is_claimable":false,"name":"ACAGT-007a, an ERK MAPK Signaling Modulator, in Combination with AKT Signaling Inhibition Induces Apoptosis in KRAS Mutant Pancreatic Cancer T3M4 and MIA-Pa-Ca-2 Cells.","description":"The mitogen-activated protein kinase (MAPK)/ERK and phosphatidylinositol-3 kinase (PI3K)/AKT pathways are dysregulated in various human cancers, including pancreatic ductal adenocarcinoma (PDAC), which has a very poor prognosis due to its lack of efficient therapies. We have previously identified ACAGT-007a (GT-7), an anti-cancer compound that kills ERK-active melanoma cells by inducing ERK-dependent apoptosis. Here, we investigated the apoptosis-inducing effect of GT-7 on three PDAC cell lines and its relevance with the MAPK/ERK and PI3K/AKT signaling pathways. GT-7 induced apoptosis in PDAC cells with different KRAS mutations (MIA-Pa-Ca-2 (KRAS G12C), T3M4 (KRAS Q61H), and PANC-1 (KRAS G12D)), being T3M4 most susceptible, followed by MIA-Pa-Ca-2, and PANC-1 was most resistant to apoptosi","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 Feb","modification":"2026-06-19T03:20:33.536Z","creation":"2025-04-19T09:45:29.734Z"},"accession":"S-EPMC8869916","cross_references":{"pubmed":["35203351"],"doi":["10.3390/cells11040702"]}}