{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["New M"],"funding":["Cancer Research UK","Versus Arthritis","The Francis Crick Institute","Medical Research Council","Wellcome Trust","Biotechnology and Biological Sciences Research Council"],"pagination":["1884-1898"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC6522344"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["79(8)"],"pubmed_abstract":["Pancreatic ductal adenocarcinoma (PDAC) is driven by metabolic changes in pancreatic cells caused by oncogenic mutations and dysregulation of p53. PDAC cell lines and PDAC-derived xenografts grow as a result of altered metabolic pathways, changes in stroma, and autophagy. Selective targeting and inhibition of one of these may open avenues for the development of new therapeutic strategies. In this study, we performed a genome-wide siRNA screen in a PDAC cell line using endogenous autophagy as a readout and identified several regulators of autophagy that were required for autophagy-dependent PDAC cell survival. Validation of two promising candidates, MPP7 (MAGUK p55 subfamily member 7, a scaffolding protein involved in cell-cell contacts) and MDH1 (cytosolic Malate dehydrogenase 1), revealed"],"journal":["Cancer research"],"pubmed_title":["MDH1 and MPP7 Regulate Autophagy in Pancreatic Ductal Adenocarcinoma."],"pmcid":["PMC6522344"],"funding_grant_id":["C596/A17196","15153","22903","BBS/E/T/000PR9819","BBS/E/F/000PR10355","FC001187","BB/J004529/1","10008","FC001999","15816","BB/P016774/1","FC001039","10187","S_3355","BBS/E/F/00044500","10006","10039"],"pubmed_authors":["Van Acker T","Long J","Tooze SA","Jiang M","Ryan KM","Sakamaki JI","Saunders RE","Behrens A","Wang VM","Jefferies HBJ","New M","Cerveira J","Korcsmaros T","Howell M","Sudhakar P"],"additional_accession":[]},"is_claimable":false,"name":"MDH1 and MPP7 Regulate Autophagy in Pancreatic Ductal Adenocarcinoma.","description":"Pancreatic ductal adenocarcinoma (PDAC) is driven by metabolic changes in pancreatic cells caused by oncogenic mutations and dysregulation of p53. PDAC cell lines and PDAC-derived xenografts grow as a result of altered metabolic pathways, changes in stroma, and autophagy. Selective targeting and inhibition of one of these may open avenues for the development of new therapeutic strategies. In this study, we performed a genome-wide siRNA screen in a PDAC cell line using endogenous autophagy as a readout and identified several regulators of autophagy that were required for autophagy-dependent PDAC cell survival. Validation of two promising candidates, MPP7 (MAGUK p55 subfamily member 7, a scaffolding protein involved in cell-cell contacts) and MDH1 (cytosolic Malate dehydrogenase 1), revealed","dates":{"release":"2019-01-01T00:00:00Z","publication":"2019 Apr","modification":"2025-04-04T02:39:25.6Z","creation":"2019-10-18T07:02:39Z"},"accession":"S-EPMC6522344","cross_references":{"pubmed":["30765601"],"doi":["10.1158/0008-5472.can-18-2553","10.1158/0008-5472.CAN-18-2553"]}}