title: Influence of gefitinib and erlotinib on apoptosis and c-MYC expression in H23 lung cancer cells.
abstract: BACKGROUND
  Gefitinib and erlotinib are inhibitors of epidermal growth factor receptor tyrosine kinase. The effects of these tyrosine kinase inhibitors on RAS-mutated cancer cells are unclear.
  
  
  METHODS
  Influence of gefitinib and erlotinib treatment was examined in H23 adenocarcinoma and A431 epidermoid carcinoma cells. The WST-1 assay was performed for evaluating cell growth. The phosphorylation status of extracellular-signal-regulated kinases (ERK) and AKT (protein kinase B) was examined by western blot. Flow cytometry was used for analyzing cell-cycle status and apoptosis detection.
  
  
  RESULTS
  In H23 cells, 20 μM erlotinib suppressed growth, while gefitinib did not suppress proliferation after 48 h of treatment. Neither gefitinib nor erlotinib affected the phosphorylation of ERK and AKT in H23 cells. Erlotinib augmented the sub-G1 population of H23 cells, while gefitinib reduced it.
  
  
  CONCLUSIONS
  In H23 cells, erlotinib accelerated apoptosis, while gefitinib induced G1 arrest.
authors.affiliation: Department of Cardiovascular, Respiratory and Metabolic Medicine, Graduate School of Medical and Dental Sciences, Kagoshima University, Kagoshima, Japan.
authors.forename: Mitsuhiro
authors.initials: M
authors.lastname: Suenaga
authors.forename: Masatatsu
authors.initials: M
authors.lastname: Yamamoto
authors.forename: Sho
authors.initials: S
authors.lastname: Tabata
authors.forename: Susumu
authors.initials: S
authors.lastname: Itakura
authors.forename: Masaaki
authors.initials: M
authors.lastname: Miyata
authors.forename: Shuichi
authors.initials: S
authors.lastname: Hamasaki
authors.forename: Tatsuhiko
authors.initials: T
authors.lastname: Furukawa
mesh_terms: D000230:Adenocarcinoma / Q000188:drug therapy / Q000378:metabolism / Q000473:pathology*; D000971:Antineoplastic Combined Chemotherapy Protocols / Q000494:pharmacology*; D017209:Apoptosis / Q000187:drug effects*; D015153:Blotting, Western; D002453:Cell Cycle / Q000187:drug effects; D049109:Cell Proliferation / Q000187:drug effects; D000069347:Erlotinib Hydrochloride; D048049:Extracellular Signal-Regulated MAP Kinases / Q000235:genetics / Q000378:metabolism; D000077156:Gefitinib; D015972:Gene Expression Regulation, Neoplastic / Q000187:drug effects*; D006801:Humans; D008175:Lung Neoplasms / Q000188:drug therapy / Q000378:metabolism / Q000473:pathology*; D010766:Phosphorylation / Q000187:drug effects; D051057:Proto-Oncogene Proteins c-akt / Q000235:genetics / Q000378:metabolism; D016271:Proto-Oncogene Proteins c-myc / Q000235:genetics / Q000378:metabolism*; D011799:Quinazolines / Q000008:administration & dosage; D012333:RNA, Messenger / Q000235:genetics; D060888:Real-Time Polymerase Chain Reaction; D020133:Reverse Transcriptase Polymerase Chain Reaction; D014407:Tumor Cells, Cultured
chemical_list: C489427:MYC protein, human; D016271:Proto-Oncogene Proteins c-myc; D011799:Quinazolines; D012333:RNA, Messenger; D000069347:Erlotinib Hydrochloride; D051057:Proto-Oncogene Proteins c-akt; D048049:Extracellular Signal-Regulated MAP Kinases; D000077156:Gefitinib