摘要
背景: 咖啡酸苯乙酯(CAPE)是蜂胶的一种活性提取物,最近有报道称它在各种癌症中有广泛的应用。然而,CAPE对小细胞肺癌(SCLC)的影响在很大程度上尚不清楚。因此,本研究的目的是通过高通量测序和生物信息学分析,确定CAPE的抗增殖作用,并探讨其在SCLC细胞中的潜在分子机制。 方法: 用CAPE治疗H446小细胞肺癌细胞,观察细胞增殖和凋亡情况。此外,在生物信息学分析中探索了miR-3960在CAPE治疗后的调控作用,并预测了改变的信号通路。 结果: CAPE明显抑制细胞增殖,诱导细胞凋亡。CAPE降低了yeah相关蛋白1 (YAP1)和细胞髓细胞增生癌基因(c-MYC)蛋白的表达。此外,CAPE上调miR-3960有助于cap诱导的细胞凋亡。miR-3960的敲除降低了cap诱导的细胞凋亡。 结论: 我们通过获得CAPE处理细胞的全面转录组图谱,证明了CAPE在人SCLC细胞中的抗癌作用,并研究其机制。
关键词: 咖啡酸苯乙酯
图形摘要
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