ArticleZhongguo fei ai za zhi = Chinese journal of lung cancer2015
[Sequence-dependent Effect of Triptolide with Gefitinib on the Proliferation and Apoptosis of Lung Adenocarcinoma Cell H1975].
Article in Zhongguo fei ai za zhi = Chinese journal of lung cancer, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundEpidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs) show promising therapeutic effects in patients with advanced non-small cell lung cancer (NSCLC). However, despite an initial response to TKIs treatment among responsive patients, most inevitably acquire resistance after a progression-free period of about 10 months. The percentage of T790M in TKI acquired-resistant patients in most studies is around 50%. The aim of this study is to assess the effects of the sequential administration of triptolide and geftinib on cell proliferation and apoptosis of lung adenocarcinoma cell H1975.
methodsA MTT assay was used to measure cell proliferation. The potency of the sequential administration of triptolide and geftinib were determined by isobolograms and combination index (CI). Cell apoptosis and cycle distribution were detected by flow cytometry. The Hoechst 33258 method was used to observe the apoptotic morphology. Chemical colorimetric luminescence was used to measure the caspase activity.
resultsThe results of isobolograms and CI showed that the sequential administration of triptolide following geftinib remarkably inhibited cell proliferation and cell apoptosis compared with other sequential administration models. The cycle distribution results indicated that sequential triptolide administration following geftinib blocked the cells in the G2/M phase but not in the G0/G1 phase. The activation of the Caspase-9/Caspase-3 cascade was mainly involved in the apoptotic pathway of lung adenocarcinoma cell H1975 in all sequential administration models.
conclusionsThe triptolide administration following geftinib might be a new therapeutic strategy for lung cancer with T790M mutation after having EGFR-TKIs resistance. .
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