期刊
THORACIC CANCER
卷 8, 期 4, 页码 296-303出版社
WILEY
DOI: 10.1111/1759-7714.12441
关键词
Binding immunoglobulin protein; caspase-9; cytochrome C; Tanshinone IIA
资金
- Technology Innovation Team of Zhengzhou [121PCXTD520]
- Research Nursery Project of Henan University of Traditional Chinese Medicine [MP2015-10]
- Doctoral Scientific Research Foundation of Henan University of Chinese Medicine [BSJJ2015-06]
BackgroundPrevious studies have shown that Tanshinone (Tan) IIA exerts obvious antitumor efficacy; however, its molecular mechanism remains unclear. This study was conducted to identify the influence of Tan IIA on Eca-109 cell apoptosis, explore its molecular mechanism, and provide a theoretical basis for clinical application. MethodsEca-109 cells were cultured in vitro and treated with different concentrations of Tan IIA. Morphologic changes were viewed under inverted fluorescence microscope with dual acridine orange/ethidium bromide staining assay. Methyl-thiazolyl-tetrazolium and Annexin V propidium iodide assays were respectively used to measure cell viability and apoptosis rate. The protein and messenger (m)RNA expression of binding immunoglobulin protein (BIP), mitochondrial cytochrome c (CytC), and caspase-9 were detected by Western blot and quantitative real-time PCR, respectively. ResultsCell viability decreased and the apoptosis rate significantly increased with increasing concentrations of Tan IIA (0, 20, 40, 60g/mL), which indicated that Tan IIA inhibited the proliferation and induced the apoptosis of Eca-109 cells in a dose-dependent manner. Eca-109 cells treated with 60g/mLTan IIA showed typical morphological changes of apoptosis under the inverted microscope. Moreover, compared with the negative control group, protein and mRNA expression of BIP decreased significantly (P< 0.05), whereas protein and mRNA expression of CytC and caspase-9 increased significantly (P< 0.05). ConclusionTan IIA can induce apoptosis in human esophageal carcinoma Eca-109 cells by regulating BIP, CytC, and caspase-9 expression. Endoplasmic reticulum stress and mitochondrial-dependent may be involved in Tan IIA-induced Eca-109 cell apoptosis.
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