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阻断ATR-SerRS-VEGFA通路针对UV诱导皮肤状细胞癌的血管生成

Hongyan Lu¹, Zhangsong Peng², Zhaohui Zheng¹

¹Department of Dermatology and Venereology, Nanfang Hospital, Southern Medical University, Guangzhou, China.

Molecular carcinogenesis

|May 2, 2024

概括

紫外线辐射 (UVR) 在皮肤癌中增加了血管内皮细胞生长因子A (VEGFA). 将埃莫丁与ATR抑制剂结合,有效地降低VEGFA,抑制皮肤状细胞癌 (cSCC) 的瘤生长和血管生成.

科学领域:

在瘤学瘤学.
皮肤病学皮肤病学
分子生物学分子生物学

背景情况:

皮肤状细胞癌 (cSCC) 是一种具有转移潜力的流行性皮肤癌.
紫外线辐射 (UVR) 是主要的危险因素,与血管内皮生长因子A (VEGFA) 表达的增加有关.
维格法在瘤血管生成和进展中起着至关重要的作用.

研究的目的:

研究cSCC中UVR诱导的VEGFA上调调节的机制.
探索针对ATR/SerRS/VEGFA通路的组合治疗策略.
评估埃莫丁和ATR抑制剂在抑制cSCC生长和血管生成方面的疗效.

主要方法:

暴露在紫外线辐射下的A431cSCC细胞,并用emodin和/或ATR抑制剂进行治疗.
分析了VEGFA表达和SerRS酸化.
在使用组合治疗的老鼠异种移植模型中评估瘤生长和血管生成.

主要成果:

紫外线治疗显著增加了A431细胞中的SerRS酸化和VEGFA表达.
埃莫丁治疗抑制了UV诱导的VEGFA表达.
与埃莫丁和ATR抑制剂的联合疗法在体外和体内表现出增强的VEGFA抑制,血管生成和瘤生长.

结论:

紫外线通过ATR/SerRS通路对cSCC中的VEGFA进行上调,促进血管生成.
血清-tRNA合成酶 (SerRS) 被确定为cSCC的新型治疗标.
埃莫丁和ATR抑制剂的联合治疗显示出抑制cSCC进展和血管生成的显著潜力.

关键词:

这是一种ATR抑制剂.这就是SerRSRS的意义.紫外线紫外线紫外线皮肤状细胞癌瘤埃莫丁是一种催产素.

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