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将LEDGF/p75过度表达与微卫星不稳定性和KRAS突变联系起来:结肠直肠癌小规模研究

Victoria Liedtke¹, Thomas Wartmann², Wenjie Shi²

¹Faculty Environment and Natural Sciences, Brandenburg University of Technology Cottbus-Senftenberg, Senftenberg, Germany.

Cancer control : journal of the Moffitt Cancer Center

|February 18, 2025

概括

75kDa的透镜表皮衍生生增长因子拼接变体 (LEDGF/p75) 在结直肠癌 (CRC) 中被上调,与KRAS和MSH2突变相关. 这一发现表明LEDGF/p75作为早期CRC检测和个性化治疗的潜在生物标志物.

科学领域:

在瘤学瘤学.
分子生物学分子生物学
遗传学遗传学是一个

背景情况:

结肠直肠癌 (CRC) 是全球癌症相关死亡的主要原因,预计发病率将增加.
早期发现和识别新生物标志物对于改善患者的治疗结果至关重要.
75kDa的透镜表皮衍生生增长因子拼接变体 (LEDGF/p75) 被认为是一种与压力相关的瘤基因.

研究的目的:

研究结直肠癌组织中LEDGF/p75和UBC13的表达水平.
分析LEDGF/p75表达和CRC患者的特定基因突变 (KRAS,MSH2) 之间的相关性.
评估LEDGF/p75作为结直肠癌预后生物标志物的潜力.

主要方法:

在15个结直肠癌 (CRC) 组织样本和相邻的非瘤组织上进行了西部斑分析,以评估蛋白质表达.
来自癌症基因组图谱 (TCGA) 数据库的521个患者样本的mRNA表达数据被用于验证.
在蛋白质分析之前,对所有患者样本进行了基于下一代测序 (NGS) 的突变分析.

主要成果:

与邻近组织相比,LEDGF/p75表达在73.3% (11/15) 的瘤组织中显著升高.
信号分子降解中的关键调节剂UBC13在60.0% (9/15) 的瘤组织中也增加了.
在LEDGF/p75过度表达和KRAS (75%) 和MSH2 (100%) 突变之间观察到强烈的相关性,在6/6名患者中观察到共过度表达.

结论:

这项研究证实了LEDGF/p75在结直肠癌中的上调,以及它与KRAS和MSH2突变的关联.
LEDGF/p75与DNA损伤反应蛋白的相互作用可能会导致药物耐药性和瘤的攻击性.
LEDGF/p75显示出作为个性化CRC治疗的独立预后生物标志物的潜力,需要进一步研究治疗向.

关键词:

修复DNA的修复DNA的修复在LEDGF/p75中使用.生物标志物生物标志物结肠直肠癌是什么意思个性化治疗是个性化的治疗.

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