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Updated: Jul 1, 2025

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解锁黑色素瘤抑制:通过PI3K-AKT-ZEB1轴从等离子体诱导的强性小RNA的洞察
Pradeep Bhartiya1, Apurva Jaiswal2, Manorma Negi2
1Plasma Bioscience Research Center, Department of Electrical and Biological Physics, Kwangwoon University, Seoul 01897, Republic of Korea; Department of Biotechnology, College of Engineering, The University of Suwon, Hwaseong 18323, Republic of Korea.
Journal of advanced research
|March 6, 2024
概括
非热大气压等离子体 (NTP) 通过改变微RNA (miRNA) 表达来有效抑制黑色素瘤,准PI3K-AKT-ZEB1等关键途径以抑制细胞生长和迁移.
科学领域:
- 在瘤学瘤学.
- 生物物理学的生物物理.
- 分子生物学分子生物学
背景情况:
- 黑色素瘤是一种高度恶性皮肤癌,尽管有针对性和免疫疗法的进展,但它仍然存在治疗挑战.
- 非热大气压等离子体 (NTP) 被探索为一种新的组合疗法,以克服化学阻力.
- 微RNAs (miRNAs) 在NTP介导的黑色素瘤细胞死亡中的作用仍然在很大程度上未被描述.
研究的目的:
- 研究NTP诱导的黑色素瘤细胞中氧化应激影响的分子机制和miRNA网络.
- 确定由NTP调节的特定miRNA及其对黑色素瘤细胞行为的影响.
主要方法:
- 黑色素瘤细胞被NTP处理,并使用高通量miRNA测序进行分析.
- 细胞活力,迁移和增殖通过Alamar Blue,酸 (PI) 摄入量和克隆基因分析进行了评估.
- 使用定量逆转录PCR (qRT-PCR) 和流细胞测量来验证miRNA和基因表达.
主要成果:
- 短时间的NTP暴露 (3分钟) 调节了miRNA表达和抑制了细胞生长.
- 长时间的NTP暴露 (5分钟) 导致显著的miRNA调节,增加PI吸收,并诱导细胞循环停止和死亡.
- miR-200b-3p和miR-215-5p的升高与黑色素瘤细胞活力和迁移的降低相关.
- 在SK-2细胞中抑制这些miRNA增加了ZEB1,PI3K和AKT的表达,促进了增殖.
结论:
- 暴露于NTP,特别是5分钟,可以差异调节PI3K-AKT-ZEB1信号通路中的miRNAs.
- NTP诱导细胞循环失调,有助于抑制黑色素瘤.
- 这项研究阐明了在黑色素瘤治疗中用于NTP的新型miRNA介导机制.
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