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Honokiol-induced apoptosis and autophagy in glioblastoma multiforme cells

机译:厚朴酚诱导胶质母细胞瘤多形细胞的凋亡和自噬

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摘要

Honokiol, a hydroxylated biphenyl compound isolated from the Chinese herb Magnolia officinalis, has been reported to have anticancer activities in a variety of cancer cell lines. The present study aimed to evaluate the anticancer effect and possible molecular mechanisms of honokiol in a glioblastoma multiforme (GBM) cell line. The anticancer activities of honokiol were investigated in the DBTRG-05MG GBM cell line. The effect of honokiol on cell growth was determined using a sulforhodamine B assay. Flow cytometry and immunoblotting were used to measure honokiol-induced apoptosis (programmed cell death type I) and autophagy (programmed cell death type II). Honokiol was observed to reduce DBTRG-05MG cell viability in a dose-dependent manner. At a dose of 50 μM, honokiol markedly decreased the expression of Rb protein and led to the cleavage of poly(ADP-ribose) polymerase and Bcl-xL to promote apoptosis in the cancer cells. In addition, markers of autophagy, including Beclin-1 and LC3-II, were also significantly increased. In addition to apoptosis, honokiol was also able to induce autophagy in the DBTRG-05MG cells. The mechanisms that are responsible for the correlation between honokiol-induced apoptosis and autophagy require further investigation. Such efforts may provide a potential strategy for improving the clinical outcome of GBM treatment.
机译:厚朴酚是从中草药木兰中分离出来的羟基联苯化合物,据报道在多种癌细胞系中均具有抗癌活性。本研究旨在评估厚朴素在多形性胶质母细胞瘤(GBM)细胞系中的抗癌作用和可能的分子机制。在DBTRG-05MG GBM细胞系中研究了厚朴酚的抗癌活性。使用磺基罗丹明B测定法测定厚朴酚对细胞生长的影响。流式细胞仪和免疫印迹法用于测量厚朴酚诱导的细胞凋亡(程序性细胞死亡类型I)和自噬(程序性细胞死亡类型II)。观察到厚朴酚以剂量依赖性方式降低DBTRG-05MG细胞活力。在50μM剂量下,厚朴酚显着降低了Rb蛋白的表达,并导致了聚(ADP-核糖)聚合酶和Bcl-xL的裂解,从而促进了癌细胞的凋亡。此外,自噬标志物,包括Beclin-1和LC3-II,也显着增加。除了凋亡外,厚朴酚还能够诱导DBTRG-05MG细胞自噬。负责厚朴酚诱导的细胞凋亡和自噬之间的相关性的机制需要进一步研究。这样的努力可能为改善GBM治疗的临床结果提供潜在的策略。

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