RT Journal Article
SR Electronic
T1 Influence of Gefitinib and Erlotinib on Apoptosis and c-MYC Expression in H23 Lung Cancer Cells
JF Anticancer Research
JO Anticancer Res
FD International Institute of Anticancer Research
SP 1547
OP 1554
VO 33
IS 4
A1 SUENAGA, MITSUHIRO
A1 YAMAMOTO, MASATATSU
A1 TABATA, SHO
A1 ITAKURA, SUSUMU
A1 MIYATA, MASAAKI
A1 HAMASAKI, SHUICHI
A1 FURUKAWA, TATSUHIKO
YR 2013
UL http://ar.iiarjournals.org/content/33/4/1547.abstract
AB 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. Materials and 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. Conclusion: In H23 cells, erlotinib accelerated apoptosis, while gefitinib induced G1 arrest.