Oncotarget:缺氧引起的IL-32β增加有利于ROS和缺氧环境下卵巢癌细胞的存活

2017-07-31 Emma MedSci原创

研究人员调查了卵巢癌细胞中调控缺氧诱导的IL-32β稳定性的潜在机制。研究显示,IL-32β在氧化应激下减少PKCδ诱导的卵巢癌细胞凋亡,即缺氧引起的IL-32β增加有利于ROS和缺氧环境下的卵巢癌细胞存活。

白细胞介素-32(IL-32)与肿瘤的研究密切相关,PKC家族中的PKCδ对许多类型的细胞起到生长抑制或促凋亡作用,而von Hippel-Lindau(VHL)肿瘤抑制蛋白是泛素介导缺氧诱导因子-1α(HIF-1α)的E3连接酶,能够被蛋白酶体降解。

研究人员调查了卵巢癌细胞中调控缺氧诱导的IL-32β稳定性的潜在机制。研究显示,IL-32β在氧化应激下减少PKCδ诱导的卵巢癌细胞凋亡,即缺氧引起的IL-32β增加有利于ROS和缺氧环境下的卵巢癌细胞存活。

在氧气条件正常的条件下,IL-32β被VHL介导的泛素化降解。与乳腺癌细胞相似,在缺氧条件下卵巢癌细胞的IL-32β表达增加。缺氧或ROS破坏了IL-32β和VHL之间的相互作用,而IL-32β和PKCδ的作用仍继续,导致细胞因子的积累。低氧诱导IL-32β将代谢方式转移到增强的糖酵解途径,IL-32β的表达量由翻译后控制调节,而不是通过转录激活调节。低氧引发PKCδ向内质网或线粒体转位,导致氧化应激诱导的细胞凋亡,但由于缺氧刺激将IL-32β转移向内质网或线粒体,增加的IL-32β与PKCδ相互作用,抑制PKCδ介导的细胞凋亡。

原始出处:
Yong HJ, et al. Von Hippel-Lindau regulates interleukin-32β stability in ovarian cancer cells. Oncotarget. 2017 Jul 17. doi: 10.18632/oncotarget.19311.

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    2018-05-02 仁医06
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    2017-09-03 psybestwish
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    2017-08-02 yxch36
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    2017-08-02 lsndxfj
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    2017-08-01 doctorJiangchao

    继续学习。

    0

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    2017-08-01 184****9840

    学习了谢谢分享

    0