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瘤干细胞的ATM激活是瘤干细胞仿真形成的关键

Jing Xie¹, Jia Xin Tang¹, Yuan Li¹

¹Department of Pathology, the First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei 230036, Anhui, China;Intelligent Pathology Institute, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei 230036, Anhui, China.

Biomedical and environmental sciences : BES

|August 28, 2024

概括

质母细胞瘤 (GBM) 中的血管生成模拟 (VM) 与生存率低下和高酸化ATM (pATM) 水平有关. 针对ATM激活可能会改善针对GBM的抗血管生成疗法.

科学领域:

神经瘤学神经瘤学
癌症生物学癌症生物学
分子病理学分子病理学

背景情况:

血管仿真 (VM) 是质母细胞瘤 (GBM) 中的一个关键过程,由质母细胞 (GSC) 驱动.
ATAXIA-telangiectasia突变 (ATM) 激酶激活与对癌症疗法的耐药性有关.
在GBM中VM和ATM激活之间的相互作用仍然不完全理解.

研究的目的:

调查血管仿真 (VM) 和化ATM (pATM) 在质母细胞瘤 (GBM) 中表达的关系.
为了确定VM和pATM在GBM患者的预后意义.
阐明ATM在促进质瘤干细胞 (GSLCs) 中VM的作用.

主要方法:

在145个GBM标本中使用双染色和免疫组织化学分析VM和pATM表达.
在体外评估来自U87和U251细胞系的GSLCs中的VM形成和pATM水平.
调查ATM抑制 (KU55933) 和对GSLCsVM形成的敲除对VM形成的影响.

主要成果:

在38.5%和41.8%的GBM瘤中,分别观察到VM和高pATM表达.
无论是VM还是高的pATM都与减少无进展和整体存活有显著的关联.
机器人无活化或淘汰抑制了VM类网络的形成,并降低了关键分子标记物的下调 (pVEGFR-2,VE-cadherin,laminin B2).

结论:

在GBM中,VM是一个独立的负预后因素,与pATM表达有关.
建议pATM激活通过细胞外基质调制和信号通路激活来促进GBM中的VM.
ATM激活代表了一个潜在的治疗目标,以加强GBM的抗血管性策略.

关键词:

突变的阿塔克西亚 - 泰朗吉克塔西亚 (ATM)质母细胞瘤 (glioblastoma) 是一个质瘤类似干细胞的细胞.血管生成的模仿.

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