These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


PUBMED FOR HANDHELDS

Search MEDLINE/PubMed


  • Title: Influence of gefitinib and erlotinib on apoptosis and c-MYC expression in H23 lung cancer cells.
    Author: Suenaga M, Yamamoto M, Tabata S, Itakura S, Miyata M, Hamasaki S, Furukawa T.
    Journal: Anticancer Res; 2013 Apr; 33(4):1547-54. PubMed ID: 23564796.
    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. 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.
    [Abstract] [Full Text] [Related] [New Search]