School of Medical Laboratory and Biotechnology, Chung Shan Medical University, Taichung, Taiwan, ROC.
Bioorg Med Chem Lett. 2010 Oct 15;20(20):6145-8. doi: 10.1016/j.bmcl.2010.08.006. Epub 2010 Aug 6.
An ergostane type triterpenoid methylantcinate A (MAA) isolated from the fruiting bodies of Antrodia camphorata inhibited the growth of oral cancer cell lines OEC-M1 and OC-2 in a dose-dependent manner, without cytotoxic to normal oral gingival fibroblast cells. The major mechanism of growth inhibition was apoptosis induction, as shown by flow cytometric analysis of annexin V-FITC and propidium iodide staining, caspase-3 activation and DNA fragmentation. The increased expression of pro-apoptotic Bax, poly-(ADP-ribose) polymerase cleavage, and activated caspase-3 and decreased expression of anti-apoptotic Bcl-2 and Bcl-xL were also observed. These results provide the first evidence that the anti-oral cancer effects of MAA may involve a mechanism through the mitochondrial dependent pathway. Thus, results reported here may offer further impulse to the development of MAA analogues as potential chemotherapeutic targets for oral cancer complications.
从灵芝子实体中分离得到的麦角甾烷型三萜类化合物甲基茵陈色原酮 A（MAA）可剂量依赖性地抑制口腔癌细胞系 OEC-M1 和 OC-2 的生长，而对正常口腔牙龈成纤维细胞无细胞毒性。流式细胞术分析 Annexin V-FITC 和碘化丙啶染色、半胱天冬酶-3 激活和 DNA 片段化显示，生长抑制的主要机制是细胞凋亡诱导。还观察到促凋亡 Bax 的表达增加、多聚（ADP-核糖）聚合酶裂解、活化的 caspase-3 和抗凋亡 Bcl-2 和 Bcl-xL 的表达减少。这些结果首次提供了证据，表明 MAA 的抗口腔癌作用可能涉及通过线粒体依赖性途径的机制。因此，这里报道的结果可能为开发 MAA 类似物作为口腔癌并发症的潜在化学治疗靶点提供进一步的动力。
