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增加的FAM134B表达会在肝细胞癌中诱导辐射敏感性

Binhui Xie¹, Yuankang Xie¹, Cuifu Fang²

¹Department of Hepatobiliary Surgery, the First Affiliated Hospital of Gannan Medical University, 341000, Ganzhou, P R China.

|July 17, 2023

概括

具有序列相似性的家族134成员B (FAM134B) 在肝细胞癌 (HCC) 中是下调调的,增加了辐射抵抗力. 恢复FAM134B或抑制JAK/Stat3可以提高HCC的放射疗效.

科学领域:

在瘤学瘤学.
分子生物学分子生物学
放射治疗研究放射治疗研究

背景情况:

已知家族与序列相似性134成员B (FAM134B) 在恶性瘤中的作用,但其在肝细胞癌 (HCC) 放射治疗耐药性中的功能尚不清楚.
澄清FAM134B在HCC中的机制可以确定克服治疗耐药性的生物标志物.

研究的目的:

调查FAM134B在HCC放射治疗耐药性的作用和分子机制.
确定FAM134B是否可以作为预测或克服HCC中放射治疗耐药性的生物标志物.

主要方法:

实时PCR和西部斑点来评估FAM134B表达.
免疫组织化学 (IHC) 用于将FAM134B与患者特征相关联.
在体外和体外功能测试 (例如细胞活力,细胞亡) 来评估FAM134B的致癌作用.
路西法酶试验阐明了涉及JAK/Stat3信号的分子机制.

主要成果:

发现FAM134B在HCC下调,与增加的辐射抵抗相关.
过度表达FAM134B使HCC细胞对辐射敏感,而抑制导致抵抗.
FAM134B与FLT3相互作用,其下调可以激活JAK/Stat3通路.
抑制JAK/Stat3抵消了FAM134B下调诱导的耐药性,并提高了治疗疗效.

结论:

通过JAK/Stat3路径,FAM134B下调促进了HCC的放射电阻.
FAM134B代表了一种潜在的治疗生物标志物,用于增强HCC患者的放射治疗.

关键词:

在FAM134B中.FLT3 FLT3 在线播放在HCC中,HCC是HCC.在JAK/Stat3信号通道上.抗辐射疗法的耐药性

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