PT  - JOURNAL ARTICLE
AU  - MITSUHIRO SUENAGA
AU  - MASATATSU YAMAMOTO
AU  - SHO TABATA
AU  - SUSUMU ITAKURA
AU  - MASAAKI MIYATA
AU  - SHUICHI HAMASAKI
AU  - TATSUHIKO FURUKAWA
TI  - Influence of Gefitinib and Erlotinib on Apoptosis and c-MYC Expression in H23 Lung Cancer Cells
DP  - 2013 Apr 01
TA  - Anticancer Research
PG  - 1547--1554
VI  - 33
IP  - 4
4099  - http://ar.iiarjournals.org/content/33/4/1547.short
4100  - http://ar.iiarjournals.org/content/33/4/1547.full
SO  - Anticancer Res2013 Apr 01; 33
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.