Macrolides sensitize EGFR-TKI-induced non-apoptotic cell death via blocking autophagy flux in pancreatic cancer cell lines - MUKAI, SHUNTARO; MORIYA, SHOTA; HIRAMOTO, MASAKI; KAZAMA, HIROMI; KOKUBA, HIROKO; CHE, XIAO-FANG; YOKOYAMA, TOMOHISA; SAKAMOTO, SATOSHI; SUGAWARA, AKIHIRO; SUNAZUKA, TOSHIAKI; ŌMURA, SATOSHI; HANDA, HIROSHI; et al. (International journal of oncology, 2016)
Keywords: Antibiotics; Apoptosis; Apoptosis - drug effects; Autophagy; Autophagy (Cytology); Autophagy - drug effects; Autophagy - genetics; Azithromycin - administration & dosage; Cancer therapies; Cell death; Cell Line, Tumor; Chemical industry; Chemotherapy; Clarithromycin - administration & dosage; Cytotoxicity; Development and progression; Drug Synergism; EGFR; Enzymes; ER stress; Erythromycin - administration & dosage; Erythromycin - analogs & derivatives; gefitinib; Gene Expression Regulation, Neoplastic - drug effects; Genetic aspects; Growth factors; Health aspects; Humans; Inhibitor drugs; Kinases; Leukemia; Lung cancer; Macrolide antibiotics; macrolides; Macrolides - administration & dosage; Medical prognosis; Metabolism; Mitochondria; Multiple myeloma; necroptosis; Pancreatic cancer; Pancreatic Neoplasms - drug therapy; Pancreatic Neoplasms - genetics; Pancreatic Neoplasms - pathology; Phosphorylation; Proteins; Quinazolines - administration & dosage; Receptor, Epidermal Growth Factor - antagonists & inhibitors; Receptor, Epidermal Growth Factor - genetics; Regulation