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摘要:
Cancer is a major public health problem throughout the world. It is estimated that one third of the American population will develop the disease at some time during their lifetimes. Among these, melanoma will account for 7% of the cases. In Brazil, in 2012, it is estimated that over six thousand new melanoma cases occurred. During recent years, the incidence of melanoma has increased, mainly due to a more constant exposure of the skin to sunlight. In this work, our aim is to assess the expression of apoptotis-related genes melanoma tumors in mice treated with Viscum album (VA). This will allow us to better understand the molecular mechanisms underlying tumor cell death activation caused by this compound. Our results clearly demonstrate upregulation of pro apoptotic genes (Trp53bp2, Nol3, Fadd, Tnfsf10, Traf1, Traf2, Cflar, Card10, Nod1, Casp 2, Casp7, Xiap, Dad1, and Dffb). Further bioinformatics-based tool analysis allowed us to assess which specific cell death-related intracellular pathways were activated by VA treatment. Two major effects of VA in melanoma cells could be observed: generation of an immunomudulatory Th-1 like action, recruiting several interleukines, and cell death activation through Caspase7, associated uspstream with Card10 and downstream with CAD. In summary, VA modulates apoptosis related genes in cancer melanoma cells. Although a deeper study should be conducted, VA seems to interfere with important signaling pathways within melanoma cells that control the cellular mechanisms of apoptosis activation. Therapeutic approaches using VA as an antineoplastic and adjuvant medication compounding should be considered.
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篇名 Viscum Album Modulates Apoptotic Related Genes in Melanoma Tumor of Mice
来源期刊 美国分子生物学期刊(英文) 学科 医学
关键词 Viscum ALBUM MELANOMA Apoptosis PATHWAYS PCR ARRAY IMMUNOHISTOCHEMISTRY
年,卷(期) 2014,(2) 所属期刊栏目
研究方向 页码范围 49-58
页数 10页 分类号 R73
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Viscum
ALBUM
MELANOMA
Apoptosis
PATHWAYS
PCR
ARRAY
IMMUNOHISTOCHEMISTRY
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研究来源
研究分支
研究去脉
引文网络交叉学科
相关学者/机构
期刊影响力
美国分子生物学期刊(英文)
季刊
2161-6620
武汉市江夏区汤逊湖北路38号光谷总部空间
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191
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0
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