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miR-211 在蛇床子提取物诱导的 ROS/ER 应激介导的 U937 和 U266 细胞凋亡中起关键作用。

miR-211 Plays a Critical Role in Cnidium officinale Makino Extract-Induced, ROS/ER Stress-Mediated Apoptosis in U937 and U266 Cells.

机构信息

Department of Pathology, College of Korean Medicine, Graduate School, Kyung Hee University, 1 Hoegi-dong, Dongdaemun-gu, Seoul 130-701, Korea.

Department of Science in Korean Medicine, College of Korean Medicine, Graduate School, Kyung Hee University, 1 Hoegi-dong, Dongdaemun-gu, Seoul 130-701, Korea.

出版信息

Int J Mol Sci. 2018 Mar 15;19(3):865. doi: 10.3390/ijms19030865.

DOI:10.3390/ijms19030865
PMID:29543750
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5877726/
Abstract

Though Makino (COM) was known to have anti-angiogenic, anti-oxidant, neuroprotective, and anti-cancer effects, the underlying anticancer mechanism of COM using endoplasmic reticulum (ER) stress and miRNA remained unclear until now. Thus, in the current study, the inhibitory mechanism of COM in lymphoma and multiple myeloma (MM) cells was elucidated. COM exerted cytotoxicity in U937 and U266 but not Raw264.7 cells. COM treatment increased the expression of ER stress-related proteins such as p-protein kinase RNA-like endoplasmic reticulum kinase (p-PERK), p-eukaryotic initiation factor (p-eIF2α), and activating transcription factor 4 (ATF4) and C/EBP homologous protein (CHOP). COM also cleaved poly (ADP-ribose) polymerase (PARP) in a dose-dependent manner in both cells. Also, reactive oxygen species (ROS) generation was elevated by COM treatment. Conversely, the apoptotic effect of COM treatment was blocked by -acetyl-l-cysteine (NAC) pretreatment. Also, the pro-survival miRNA, miR-211 was decreased by COM treatment in U937 and U266 cells. miR-211 mimic attenuated COM-induced apoptosis. Taken together, these results support the scientific evidence that COM induces apoptosis via ROS generation/CHOP activation and miR-211 suppression in U937 and U266 cells.

摘要

尽管 Makino（COM）已被证实具有抗血管生成、抗氧化、神经保护和抗癌作用，但直到现在，COM 通过内质网（ER）应激和 miRNA 发挥抗癌作用的潜在机制仍不清楚。因此，在本研究中，阐明了 COM 对淋巴瘤和多发性骨髓瘤（MM）细胞的抑制机制。COM 对 U937 和 U266 细胞具有细胞毒性，但对 Raw264.7 细胞没有。COM 处理增加了 ER 应激相关蛋白的表达，如 p-蛋白激酶 RNA 样内质网激酶（p-PERK）、p-真核起始因子（p-eIF2α）和激活转录因子 4（ATF4）和 C/EBP 同源蛋白（CHOP）。COM 还以剂量依赖的方式在两种细胞中切割聚（ADP-核糖）聚合酶（PARP）。此外，COM 处理会增加活性氧（ROS）的产生。相反，COM 处理的细胞凋亡作用被乙酰-l-半胱氨酸（NAC）预处理阻断。此外，COM 处理降低了 U937 和 U266 细胞中促生存 miRNA miR-211 的表达。miR-211 模拟物减弱了 COM 诱导的细胞凋亡。综上所述，这些结果支持 COM 通过 ROS 生成/CHOP 激活和 miR-211 抑制诱导 U937 和 U266 细胞凋亡的科学证据。

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