LncRNA SPRY4-IT1通过DUSP6-ERK1/2-Chk1信号通路调节由颗粒物诱导的16HBE细胞恶性转变
Yanli Li1, Dan Tang1, Jian Zhang1
1State Key Laboratory of Respiratory Disease, Institute for Chemical Carcinogenesis, Guangzhou Medical University, Guangzhou, 511436, PR China.
Chemosphere
|October 5, 2023
概括
暴露于颗粒物会通过改变细胞功能触发肺癌. 该研究发现,长非编码RNA SPRY4-IT1 作为瘤抑制剂,通过调节DUSP6-ERK1/2-Chk1通路来逆转这些有害影响.
科学领域:
- 环境健康 环境健康
- 分子生物学分子生物学
- 癌症研究 癌症研究
背景情况:
- 颗粒物 (PM) 是主要的空气污染物,与呼吸道疾病,包括肺癌有关.
- 长非编码RNAs (lncRNAs) 与癌症发展有关,但它们在PM诱导的肺癌发生中的作用尚未完全理解.
研究的目的:
- 研究lncRNAs在PM诱导的16HBE细胞恶性转化中的作用和机制.
- 为了确定涉及PM诱导细胞变化的特定lncRNAs.
主要方法:
- 使用20μg/ml的PM,建立了一个PM转化16HBE细胞模型 (PM-T细胞).
- 与对照16HBE细胞相比,PM-T细胞的差异性基因表达和功能变化 (增殖,迁移,细胞周期,细胞亡) 的分析.
- 识别的 lncRNAs 的过度表达,以评估它们对细胞功能和信号通路的影响.
主要成果:
- PM-T细胞表现出改变的生物功能,包括增加的增殖,迁移和细胞周期进展,随着细胞亡的减少.
- 在PM-T细胞中,LncRNA SPRY4-IT1显著下调,其过度表达逆转了观察到的功能变化.
- 发现LncRNA SPRY4-IT1通过负调节DUSP6-ERK1/2通路来调节Chk1的表达.
结论:
- 在PM诱导的肺癌发生的背景下,LncRNA SPRY4-IT1充当瘤抑制基因.
- SPRY4-IT1通过DUSP6-ERK1/2-Chk1信号通路调解16HBE细胞的恶性转化.
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