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通过 miR-508/ZWINT 轴通过 LncRNA AFAP-AS1 调节人类肺腺癌细胞增殖
Sultan F Kadasah1, Abdulaziz M S Alqahtani1
1Department of Biology, Faculty of Science, University of Bisha, P.O. Box 551, Bisha 61922, Saudi Arabia.
International journal of molecular sciences
|July 12, 2025
概括
长非编码RNAAFAP1-AS1通过增加细胞增殖和侵入来促进肺腺癌. 针对AFAP1-AS1或其miR-508-3p/ZWINT通路提供了潜在的新肺癌治疗方法.
科学领域:
- 在瘤学瘤学.
- 分子生物学分子生物学
- 生物化学 生物化学
背景情况:
- 肺腺癌是一种侵袭性癌症,由于早期转移和治疗耐药性,预后不佳.
- 长非编码RNA (lncRNA) AFAP1-AS1与各种癌症的进展有关.
研究的目的:
- 研究AFAP1-AS1在肺腺癌细胞增殖,亡和侵袭中的功能作用.
- 阐明涉及miR-508-3p/ZWINT轴的潜在分子机制.
主要方法:
- 在使用siRNA的A549肺腺癌细胞中抑制AFAP1-AS1表达.
- 评估细胞增殖 (CCK-8,殖民地形成),细胞亡 (AO/EB染色,Bax/Bcl-2表达) 和入侵 (Transwell测定).
- 通过双 luciferase 记者测定和 qRT-PCR 确认分子相互作用.
主要成果:
- 在肺腺癌细胞中,AFAP1-AS1被显著上调.
- 沉默AFAP1-AS1减少了细胞增殖,殖民地形成和入侵,同时增加了细胞亡.
- AFAP1-AS1与针对ZWINT的miR-508-3p直接相互作用;ZWINT过度表达逆转了AFAP1-AS1沉默的影响.
结论:
- AFAP1-AS1通过miR-508-3p/ZWINT途径促进肺腺癌的进展,影响细胞增殖,细胞亡和入侵.
- 准AFAP1-AS1或其下游轴为肺腺癌提供了潜在的治疗策略.
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