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纤维细胞生长因子诱导肝脏瘤发生后的射频除

Aurelia Markezana¹, Mor Paldor², Haixing Liao²

¹The Goldyne Savad Institute of Gene and Cell Therapy, Hadassah Hebrew University Hospital, Ein Karem, Jerusalem, Israel. aureliahakoune@gmail.com.

Scientific reports

|September 28, 2023

概括

肝癌的射频切除 (RFA) 可以意外地刺激瘤生长. 这项研究表明,RFA激活FGF信号通路,促进癌细胞增殖,但抑制这种通路可以抑制瘤的发展.

科学领域:

在瘤学瘤学.
肝病学肝病学是一种肝病学.
分子生物学分子生物学

背景情况:

图像引导的射频除 (RFA) 是用于肝脏瘤的常见治疗方法.
然而,具有悖论的,肝脏RFA可能通过激活前瘤原始因子来促进瘤生长.
识别和抑制这些亲瘤效应对于提高RFA疗效至关重要.

研究的目的:

调查射频除 (RFA) 可能促进瘤生长的机制.
为了确定参与RFA诱导瘤发生的特定分子途径.
评估抑制这些途径的治疗潜力.

主要方法:

评估了患者血RFA后对肝细胞癌 (HCC) 细胞系的增殖效应.
利用多重ELISA和蛋白质阵列来查亲瘤生长因子和细胞因子.
研究了纤维细胞生长因子 (FGF) 在RFA后HCC小鼠模型中信号传递的作用,测试了FGFR抑制剂.

主要成果:

与基线相比,来自RFA后患者的血显著增加了HCC细胞增殖.
在RFA后检测到高水平的FGF家族蛋白质,选择性地激活HepG2细胞.
过热诱导的肝细胞受条件介质也促进了癌细胞的增殖.
在RFA后的HCC小鼠模型中,FGFR抑制显著降低了肝脏瘤负担.

结论:

肝脏RFA可以通过激活FGF信号通路,至少部分诱导瘤发生.
准FGF受体 (FGFR) 途径是一种潜在的策略,可以抑制RFA诱导的HCC发展.
对抑制FGF信号的进一步研究可能会提高RFA治疗肝癌的治疗结果.

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