Influence of gefitinib and erlotinib on apoptosis and c-MYC expression in H23 lung cancer cells
| Autor: | Mitsuhiro, Suenaga, Masatatsu, Yamamoto, Sho, Tabata, Susumu, Itakura, Masaaki, Miyata, Shuichi, Hamasaki, Tatsuhiko, Furukawa |
|---|---|
| Rok vydání: | 2013 |
| Předmět: |
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 |
| Zdroj: | Anticancer research. 33(4) |
| ISSN: | 1791-7530 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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