Stem Cells:低氧介导的脑肿瘤细胞干性的表观遗传调控

2017-04-09 MedSci MedSci原创

多能调节通路的活化是实体肿瘤进展中的重要过程,目前研究表明缺氧的微环境可以增强一些细胞的干细胞特征。癌症干细胞(CSCs)/肿瘤起始细胞(TICs)可以增加侵袭、转移和耐药性。此前有研究报道了神经胶质瘤的全球低甲基化和位点特异性异常甲基化以及其他表观遗传修饰,它们是胶质瘤进展期间基因组不稳定性的重要参与因素。近期,一项发表在杂志Stem cells上的研究证明了缺氧介导的表观遗传修饰在调节神经胶质

多能调节通路的活化是实体肿瘤进展中的重要过程,目前研究表明缺氧的微环境可以增强一些细胞的干细胞特征。癌症干细胞(CSCs)/肿瘤起始细胞(TICs)可以增加侵袭、转移和耐药性。此前有研究报道了神经胶质瘤的全球低甲基化和位点特异性异常甲基化以及其他表观遗传修饰,它们是胶质瘤进展期间基因组不稳定性的重要参与因素。


近期,一项发表在杂志Stem cells上的研究证明了缺氧介导的表观遗传修饰在调节神经胶质瘤细胞中核心多能因子OCT4和NANOG的表达中的作用。

此项研究发现,缺氧诱导了脱甲基酶,TET1和3,而不是TET2。免疫沉淀研究显示在Oct4和Nanog调节区域的去甲基化活化以及Oct4和Nanog调节区域TET1和3的直接结合。Tet1和3沉默测定进一步证实了通过这些旁路诱导的多潜能通路(包括Oct4、Nanog和Stat3)。 Tet1和Tet3的敲除抑制了缺氧条件下神经球的形成。

此项研究还发现,在缺氧条件下,TET1和TET3的多能性和分化相关基因的独立作用。

此项研究表明TET1和3作为Oct4和Nanog过表达的机制,在缺氧中有主动脱甲基的作用,从而有助于神经胶质瘤中CSCs的形成。

原始出处:
Prasad AP, Arora Mittal S, et al. Hypoxia-mediated epigenetic regulation of stemness in brain tumor cells. Stem Cells. 2017 Apr 4. doi: 10.1002/stem.2621.

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    2017-12-26 维他命
  5. 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  6. 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  7. 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    2017-04-09 1e1a50a1m36(暂无匿称)

    TET1和3作为Oct4和Nanog过表达的机制,在缺氧中有主动脱甲基的作用,从而有助于神经胶质瘤中CSCs的形成。

    0

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