TMEM2诱导了表皮-介质细胞转换,并促进了GBM细胞对temozolomide的抗性

TMEM2诱导了表皮-介质细胞转换,并促进了GBM细胞对temozolomide的抗性

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Lun Gao^1,2, Shiao Tong^1,2, Junhui Liu^1,2

¹Department of Neurosurgery, Renmin Hospital of Wuhan University, Wuhan, China.

Heliyon

|June 9, 2023

概括

转膜蛋白2 (TMEM2) 在多种质母细胞瘤 (GBM) 中被上调,与恶性瘤和降低生存率相关. 向TMEM2抑制了GBM细胞的增殖,并提高了temozolomide (TMZ) 治疗的疗效,提供了诊断和治疗潜力.

科学领域:

在瘤学瘤学.
分子生物学分子生物学
生物标志物生物标志物

背景情况:

多形质母细胞瘤 (GBM) 是一种具有侵略性的脑瘤,由于对其病变的理解有限,缺乏有效的生物标志物,预后不佳.
跨膜蛋白2 (TMEM2) 已涉及到各种人类癌症,但其在质瘤中的作用在很大程度上仍未被描述.
现有研究表明TMEM2可能预测质瘤患者的存活率,但其表达和功能意义需要进一步调查.

研究的目的:

调查TMEM2在质瘤中的表达水平和生物作用,特别是在GBM中.
确定TMEM2表达与质瘤恶性病变之间的相关性,患者存活率和对特莫佐洛米德 (TMZ) 治疗的反应.
探索TMEM2作为GBM的诊断和治疗生物标志物的潜力.

主要方法:

在公共和内部数据集中分析TMEM2表达,将GBM组织与非瘤脑组织 (NBT) 进行比较.
TMEM2表达水平与临床病理特征之间的相关性分析,包括瘤恶性和患者存活率 (Kaplan-Meier分析).
试验室内实验涉及TMEM2在GBM细胞中被淘汰,以评估对增殖,细胞亡和上皮-介质细胞过渡 (EMT) 的影响,包括跨well测定和与TMZ治疗的结合.

主要成果:

与NBT相比,在GBM组织中,TMEM2的表达显著高于NBT,并且与瘤恶性相关.
高TMEM2表达与所有质瘤患者的整体存活率降低有关,包括GBM和低度质瘤 (LGG) 患者.
TMEM2倒置抑制了GBM细胞增殖,抑制了EMT,并提高了对TMZ治疗的敏感性,导致细胞亡的增加.

结论:

TMEM2是GBM中的瘤原蛋白,促进瘤的进展,并对患者的生存产生负面影响.
TMEM2上调与GBM的介质细胞亚型有关,并与对TMZ治疗的抵抗有关.
TMEM2代表了早期诊断,预后预测和改善GBM治疗结果的潜在治疗目标的有希望的生物标志物.

关键词:

在EMT中,EMT是EMT.预测预后预测预测核武器的扩散 TMEM2 TMEM2 的意思是什么?在TMZZ上,你会看到TMZ.

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