{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Katreddy RR"],"funding":["NIA NIH HHS","NCI NIH HHS"],"pagination":["5"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC5833766"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["7(1)"],"pubmed_abstract":["The oncogenic epidermal growth factor receptor (EGFR) is commonly overexpressed in solid cancers. The tyrosine kinase activity of EGFR has been a major therapeutic target for cancer; however, the efficacy of EGFR tyrosine kinase inhibitors to treat cancers has been challenged by innate and acquired resistance at the clinic. Accumulating evidence suggests that EGFR possesses kinase-independent pro-survival functions, and that cancer cells are more vulnerable to reduction of EGFR protein than to inhibition of its kinase activity. The molecular mechanism underlying loss-of-EGFR-induced cell death remains largely unknown. In this study, we show that, unlike inhibiting EGFR kinase activity that is known to induce pro-survival non-selective autophagy, downregulating EGFR protein, either by siRNA"],"journal":["Oncogenesis"],"pubmed_title":["Targeted reduction of the EGFR protein, but not inhibition of its kinase activity, induces mitophagy and death of cancer cells through activation of mTORC2 and Akt."],"pmcid":["PMC5833766"],"funding_grant_id":["R21 AG045382","R01 CA203737"],"pubmed_authors":["Lu X","Huang G","Wu B","Bollu LR","Weihua Z","Dai Y","Zhang Q","Su F","Rea MA","Srivastava S","Xian N","Thomas R","Briggs JM","Katreddy RR","Xu Y"],"additional_accession":[]},"is_claimable":false,"name":"Targeted reduction of the EGFR protein, but not inhibition of its kinase activity, induces mitophagy and death of cancer cells through activation of mTORC2 and Akt.","description":"The oncogenic epidermal growth factor receptor (EGFR) is commonly overexpressed in solid cancers. The tyrosine kinase activity of EGFR has been a major therapeutic target for cancer; however, the efficacy of EGFR tyrosine kinase inhibitors to treat cancers has been challenged by innate and acquired resistance at the clinic. Accumulating evidence suggests that EGFR possesses kinase-independent pro-survival functions, and that cancer cells are more vulnerable to reduction of EGFR protein than to inhibition of its kinase activity. The molecular mechanism underlying loss-of-EGFR-induced cell death remains largely unknown. In this study, we show that, unlike inhibiting EGFR kinase activity that is known to induce pro-survival non-selective autophagy, downregulating EGFR protein, either by siRNA","dates":{"release":"2018-01-01T00:00:00Z","publication":"2018 Jan","modification":"2026-05-05T03:52:22.257Z","creation":"2026-04-07T21:21:13.537Z"},"accession":"S-EPMC5833766","cross_references":{"pubmed":["29358623"],"doi":["10.1038/s41389-017-0021-7"]}}