甲基磺酰甲烷诱导YD-38牙龈癌细胞G期阻滞和线粒体凋亡。
Methylsulfonylmethane Induces G Arrest and Mitochondrial Apoptosis in YD-38 Gingival Cancer Cells.
作者信息
P Nipin S, Kang Dong Young, Kim Baek Joong, Joung Youn Hee, Darvin Pramod, Byun Hyo Joo, Kim Joong Gon, Park Je Uk, Yang Young Mok
机构信息
Department of Pathology, School of Medicine, Institute of Biomedical Science and Technology, Konkuk University, Seoul, Republic of Korea.
Department of Oral and Maxillofacial Surgery, College of Medicine, The Catholic University of Korea, Seoul, Republic of Korea.
出版信息
Anticancer Res. 2017 Apr;37(4):1637-1646. doi: 10.21873/anticanres.11494.
Gingival squamous cell carcinoma is a rare form of cancer that accounts for less than 10% of all head and neck cancers. Targeted therapies with natural compounds are of interest because they possess high efficacy with fewer side-effects. Methylsulfonylmethane (MSM) is an organic sulfur-containing compound with anticancer activities. The main goal of this study was to induce proliferation inhibition and apoptosis in the metastatic YD-38 cell line. MSM up-regulated expression of P21 and P27 genes and down-regulated expression of cyclin D1 (CCND1) and CDK4. Moreover, treatment with MSM induced apoptosis and up-regulation of BAX in YD-38 cells. In accordance, the expression of the BCL-2 and BCL-XL, were inhibited, indicating the role of mitochondria in MSM-induced apoptosis. Analysis of mitochondrial integrity showed a loss of mitochondrial potential with an increased level of cytochrome c in the cytosol compared to mitochondria. Active CASPASE-3 (CASP3) was also observed, confirming that MSM-induced apoptosis is caspase-mediated.
牙龈鳞状细胞癌是一种罕见的癌症形式，占所有头颈癌的比例不到10%。天然化合物靶向疗法备受关注，因为它们疗效高且副作用少。甲基磺酰甲烷（MSM）是一种具有抗癌活性的有机含硫化合物。本研究的主要目的是诱导转移性YD-38细胞系的增殖抑制和凋亡。MSM上调P21和P27基因的表达，下调细胞周期蛋白D1（CCND1）和细胞周期蛋白依赖性激酶4（CDK4）的表达。此外，MSM处理诱导YD-38细胞凋亡并上调BAX表达。相应地，BCL-2和BCL-XL的表达受到抑制，表明线粒体在MSM诱导的凋亡中起作用。线粒体完整性分析显示线粒体电位丧失，与线粒体相比，胞质溶胶中细胞色素c水平升高。还观察到活性半胱天冬酶-3（CASP3），证实MSM诱导的凋亡是由半胱天冬酶介导的。
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