PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 23917044-6 2013 Inhibition of autophagy by chloroquine and knockdown of autophagy pathway genes Beclin-1 and Atg5 sensitized both cell lines to erlotinib-induced cytotoxicity, suggesting that autophagy may serve as a protective mechanism. Erlotinib Hydrochloride 128-137 autophagy related 5 Homo sapiens 93-97 26797786-8 2016 Then, through siRNA technology and WB, we found that erlotinib-induced autophagy is mediated by ATG5 but not Beclin1. Erlotinib Hydrochloride 53-62 autophagy related 5 Homo sapiens 96-100 26797786-9 2016 Also, knockdown of ATG5 significantly decreased the erlotinib resistance and knockdown of Beclin1 did not affect the sensitivity to erlotinib in TSCCs. Erlotinib Hydrochloride 52-61 autophagy related 5 Homo sapiens 19-23 21655094-6 2011 Moreover, cytotoxicity induced by gefitinib or erlotinib was greatly enhanced after autophagy inhibition by the pharmacological inhibitor chloroquine (CQ) and siRNAs targeting ATG5 and ATG7, the most important components for the formation of autophagosome. Erlotinib Hydrochloride 47-56 autophagy related 5 Homo sapiens 176-180 23769318-10 2013 Erlotinib treatment at clinically relevant concentrations induced autophagy (increased LC3II expression, Atg-5/Atg12 conjugation, formation of AVO and p62 degradation) in sensitive NSCLC cell lines, via p53 nuclear translocation, AMPK activation and mTOR suppression. Erlotinib Hydrochloride 0-9 autophagy related 5 Homo sapiens 105-110 23769318-12 2013 Similarly, silencing of Atg5 or Beclin-1 significantly increased sensitivity to erlotinib in both sensitive cell lines. Erlotinib Hydrochloride 80-89 autophagy related 5 Homo sapiens 24-28