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首页> 外文期刊>Journal of Cellular Physiology >S-Adenosylmethionine Affects ERK1/2 and Stat3 Pathways and Induces Apotosis in Osteosarcoma Cells
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S-Adenosylmethionine Affects ERK1/2 and Stat3 Pathways and Induces Apotosis in Osteosarcoma Cells

机译：S-Adenosylmethionine影响ERK1/2和Stat3途径和诱发Apotosis在骨肉瘤细胞

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Osteosarcoma is a very aggressive bone tumor. Its clinical outcome remains discouraging despite intensive surgery, radiotherapy, and chemotherapy. Thus, novel therapeutic approaches are demanded. S-Adenosylmethionine (AdoMet) is a naturally occurring molecule that is synthesized in our body by methionine adenosyltransferase isoenzymes and is also available as a nutritional supplement. AdoMet is the principal methyl donor in numerous methylation reactions and is involved in many biological functions. Interestingly, AdoMet has been shown to exert antiproliferative action in various cancer cells. However, the underlying molecular mechanisms are just starting to be studied. Here, we investigated the effects of AdoMet on the proliferation of osteosarcoma U2OS cells and the underlying mechanisms. We carried out direct cell number counting, MTT and flow cytometry-based assays, and immunoblotting experiments in response to AdoMet treatment. We found that AdoMet strongly inhibits proliferation of U2OS cells by slowing-down cell cycle progression and by inducing apoptosis. We also report that AdoMet consistently causes an increase of p53 and p21 cell-cycle inhibitor, a decrease of cyclin A and cyclin E protein levels, and a marked increase of pro-apoptotic Bax/Bcl-2 ratio, with caspase-3 activation and PARP cleavage. Moreover, the AdoMet-induced antiproliferative effects were dynamically accompanied by profound changes in ERK1/2 and STAT3 protein and phosphorylation levels. Altogether, our data enforce the evidence of AdoMet acting as a biomolecule with antiproliferative action in osteosarcoma cells, capable of down-regulating ERK1/2 and STAT3 pathways leading to cell cycle inhibition and apoptosis, and provide a rationale for the possible use of AdoMet in osteosarcoma therapy. J. Cell. Physiol. 231: 428-435, 2016. (c) 2015 Wiley Periodicals, Inc.
机译：骨肉瘤是一种非常激进的骨肿瘤。临床结果仍令人沮丧,尽管密集的手术、放疗和化疗。是要求。天然合成的分子在我们的身体由蛋氨酸adenosyltransferase同功酶,也可以作为营养补充。在众多的甲基化反应和参与在很多生物功能。AdoMet可以发挥抗增殖在各种癌症细胞。潜在的分子机制是刚刚开始研究了。AdoMet对骨肉瘤的扩散U2OS细胞和底层机制。直接进行细胞计数,MTT和流cytometry-based化验和免疫印迹实验针对AdoMet治疗。发现AdoMet强烈抑制增殖U2OS细胞的细胞周期的减速进展和诱导细胞凋亡。报告,AdoMet一直引起增加p53、p21细胞循环抑制剂细胞周期蛋白和细胞周期素E蛋白水平的降低,和显著增加pro-apoptotic伯灵顿/ bcl - 2比,caspase-3激活和PARP分裂抗增殖效果动态伴随着ERK1/2和深刻的变化STAT3蛋白和磷酸化水平。总之,我们的数据执行的证据AdoMet作为生物分子抗增殖作用在骨肉瘤细胞中,能够显示ERK1/2和STAT3途径导致细胞周期抑制细胞凋亡,并提供一个理由可能使用AdoMet骨肉瘤治疗。j .细胞。威利期刊公司。

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