雄激素受体抑制肺癌的侵袭,并通过降低TPD52表达来增加西斯的反应
Shiqing Liu1,2,3, Chengping Hu1,2, Min Li1,2
1Department of Respiratory Medicine, Xiangya Hospital, Central South University, Changsha, 410008, China.
International journal of biological sciences
|August 11, 2023
概括
雄激素受体 (AR) 抑制肺癌的侵袭,并通过调节circ-SLCO1B7,miR-139-5p和TPD52.p来改善西斯普拉丁的反应. 这种AR途径为非小细胞肺癌 (NSCLC) 治疗提供了潜在的新疗法策略.
科学领域:
- 在瘤学瘤学.
- 分子生物学分子生物学
- 遗传学 是一个遗传学.
背景情况:
- 肺癌仍然是全球癌症死亡的主要原因,需要新的治疗点.
- 雄激素受体 (AR) 在非小细胞肺癌 (NSCLC) 进展中的作用及其与TPD52和西斯 (DDP) 反应的相互作用需要进一步阐明.
研究的目的:
- 研究AR如何影响NSCLC细胞入侵和西斯普拉丁反应的机制.
- 探索AR/circ-SLCO1B7/miR-139-5p/TPD52信号轴在NSCLC进展中的作用.
主要方法:
- 研究了AR对NSCLC细胞入侵和DDP敏感性的影响.
- 分析了AR通过直接促进体结合对circ-SLCO1B7表达的调节.
- 研究了RNA诱导沉默复合体 (RISC) 中circ-SLCO1B7,miR-139-5p和TPD52mRNA之间的相互作用.
- 通过体内实验和对人类NSCLC数据库和临床标本分析的验证结果.
主要成果:
- 通过降低circ-SLCO1B7表达的调节,AR抑制NSCLC细胞入侵,并增强DDP反应.
- AR直接与SLCO1B7促进体结合,从而降低circ-SLCO1B7的水平.
- 减少circ-SLCO1B7释放miR-139-5p,它准TPD52mRNA,导致TPD52的表达减少.
- 证实AR/circ-SLCO1B7/miR-139-5p/TPD52途径在体内和人类样本中的肺癌进展中具有功能性作用.
结论:
- 通过circ-SLCO1B7/miR-139-5p/TPD52通路,AR作为NSCLC细胞入侵的抑制剂和DDP反应的增强剂.
- 针对这种新的AR介导信号通路,为NSCLC提供了一个有前途的治疗策略.
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