Influence of gefitinib and erlotinib on apoptosis and c-MYC expression in H23 lung cancer cells.
Copyright policy )Influence of gefitinib and erlotinib on apoptosis and c-MYC expression in H23 lung cancer cells.
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.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.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.In H23 cells, erlotinib accelerated apoptosis, while gefitinib induced G1 arrest.
- Kagoshima University Japan
Lung Neoplasms, Reverse Transcriptase Polymerase Chain Reaction, Blotting, Western, Cell Cycle, Apoptosis, Gefitinib, Adenocarcinoma, Real-Time Polymerase Chain Reaction, Gene Expression Regulation, Neoplastic, Proto-Oncogene Proteins c-myc, Erlotinib Hydrochloride, Antineoplastic Combined Chemotherapy Protocols, Quinazolines, Tumor Cells, Cultured, Humans, RNA, Messenger, Phosphorylation, Extracellular Signal-Regulated MAP Kinases, Proto-Oncogene Proteins c-akt, Cell Proliferation
Lung Neoplasms, Reverse Transcriptase Polymerase Chain Reaction, Blotting, Western, Cell Cycle, Apoptosis, Gefitinib, Adenocarcinoma, Real-Time Polymerase Chain Reaction, Gene Expression Regulation, Neoplastic, Proto-Oncogene Proteins c-myc, Erlotinib Hydrochloride, Antineoplastic Combined Chemotherapy Protocols, Quinazolines, Tumor Cells, Cultured, Humans, RNA, Messenger, Phosphorylation, Extracellular Signal-Regulated MAP Kinases, Proto-Oncogene Proteins c-akt, Cell Proliferation
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