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细胞外囊包装MIR4435-2HG 通过酶1依赖的糖溶性重编程促进香烟烟雾诱导的膀癌进展
Rui Zheng1,2,3, Yanping Xiao1, Jialei Yang1,4
1Departments of Environmental Genomics and Genetic Toxicology, The Key Laboratory of Modern Toxicology of Ministry of Education, Center for Global Health, Jiangsu Key Laboratory of Cancer Biomarkers, Prevention and Treatment, Collaborative Innovation Center for Cancer Personalized Medicine, School of Public Health, Institute of Clinical Research, The Affiliated Taizhou People's Hospital of Nanjing Medical University, Taizhou School of Clinical Medicine, Nanjing Medical University, Nanjing 211166, China.
香烟烟雾促进膀癌通过将IncRNA MIR4435-2HG包装到细胞外囊泡 (EVs) 中. 这种分子重新编程瘤细胞,并与巨细胞建立反循环,提供新的预防和治疗策略.
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:
- 吸烟是膀癌的已知危险因素,但潜在的生物机制尚不清楚.
- 细胞外囊泡 (EVs) 和长非编码RNA (lncRNAs) 涉及细胞间通信和癌症进展.
研究的目的:
- 阐明吸烟促进膀癌进展的生物机制.
- 为了识别和表征EV包装的 lncRNAs 参与膀癌症的发展,由于吸烟.
- 探索候选 lncRNAs 的临床价值和机制作用.
主要方法:
- RNA测序,组织微阵列和单细胞RNA测序以识别lncRNAs.
- 机械学研究的CRISPR/Cas9,海马测定和N4-乙基丁 (ac4C) 乙化实验.
- 来自有吸烟史的膀癌患者的尿液和血样本的分析.
主要成果:
- 确定了EV包装的lncRNAMIR4435-2HG,在暴露于4-aminobiphenyl (4-ABP) 时由M2巨分泌.
- 4-ABP诱导了M2巨细胞极化和STAT6酸化,导致FUS表达和MIR4435-2HG包装到EVs.
- 通过EVs传递的MIR4435-2HG通过ac4C修饰和miR-143-3p海绵,激活PI3K-Akt信号,通过调节糖解 (ENO1) 来重新编程受体瘤细胞.
- 建立了一个前循环,瘤细胞招募单细胞,促进M2巨细胞的两极分化.
结论:
- EV包装的MIR4435-2HG是吸烟相关的膀癌中细胞间通信的关键媒介.
- MIR4435-2HG在通过糖溶性重编程促进膀瘤发展方面发挥着关键作用.
- MIR4435-2HG作为吸烟者膀癌的潜在诊断标记物和治疗点.
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