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缺氧抑制HUNK激酶活性以诱导上皮层-介质细胞过渡
Siyuan Jiang1, Xiaoqi Han2, Zidong Zhao1
1Zhongda Hospital, Medical School, Advanced Institute for Life and Health, Southeast University, Nanjing, 210096, China.
Biochemical and biophysical research communications
|October 4, 2023
概括
缺氧影响大肠直肠癌 (CRC) 中荷尔蒙上调新相关激酶 (HUNK) 活性. 这项研究揭示了缺氧影响HANK介导的酸化,影响癌细胞迁移和入侵.
科学领域:
- 在瘤学瘤学.
- 分子生物学分子生物学
- 癌症研究 癌症研究
背景情况:
- 缺氧是癌症进展和上皮-介质细胞转变 (EMT) 的关键因素.
- 已知荷尔蒙上调新相关激酶 (HUNK) 通过其激酶活性来调节EMT.
- 低氧和HUNK在EMT中介中的相互作用在很大程度上仍未被探索.
研究的目的:
- 为了研究缺氧和HUNK激酶活性在结直肠癌 (CRC) 中的关系.
- 阐明缺氧对CRC细胞中HUNK介导信号通路的功能后果.
主要方法:
- 在低氧条件下的HUNK表达和活性在CRC细胞系中的分析.
- 对低氧反应下游蛋白质酸化的评估.
- 在不同氧气水平下评估细胞迁移,入侵和EMT标志物表达.
主要成果:
- 缺氧不会改变HUNK表达水平,而是通过改变下游蛋白质酸化直接调节其激酶活性.
- 低氧引起的CRC细胞中迁移,入侵和EMT标记物的上调,部分是由减少的HUNK活动调节的.
- HUNK酸化的特定下游目标受到低氧条件的影响.
结论:
- 缺氧和HUNK激酶活性在结直肠癌EMT的背景下是密切相关的.
- 缺氧影响HUNK介导的信号传递,影响癌细胞的攻击性.
- 准HUNK-低氧轴为抑制CRC转移提供了一个潜在的治疗策略.
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