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阿魏酸苯乙酯和咖啡酰胺衍生物抑制口腔鳞状细胞癌细胞。

Caffeic Acid Phenethyl Ester and Caffeamide Derivatives Suppress Oral Squamous Cell Carcinoma Cells.

机构信息

Department of Healthcare Administration, Asia University, Taichung 41354, Taiwan.

School of Dentistry, China Medical University, Taichung 40402, Taiwan.

出版信息

Int J Mol Sci. 2023 Jun 6;24(12):9819. doi: 10.3390/ijms24129819.

DOI:10.3390/ijms24129819
PMID:37372967
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10298160/
Abstract

Caffeic acid phenethyl ester (CAPE) contains antibiotic and anticancer activities. Therefore, we aimed to investigate the anticancer properties and mechanisms of CAPE and caffeamide derivatives in the oral squamous cell carcinoma cell (OSCC) lines SAS and OECM-1. The anti-OSCC effects of CAPE and the caffeamide derivatives (, , , , and ) were evaluated using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide test. Cell cycle and total reactive oxygen species (ROS) production were analyzed using flow cytometry. The relative protein expression of malignant phenotypes was determined via Western blot analysis. The results showed that and were more cytotoxic than the other compounds in SAS cells. After or treatment for 48 h, cell cycle S phase or G2/M phase arrest was induced, and cellular ROS increased at 24 h, and then decreased at 48 h in both cell lines. The expression levels of cell cycle regulatory and anti-ROS proteins were downregulated. In addition, or treatment inhibited malignant phenotypes through mTOR-ULK1-P62-LC3 autophagic signaling activated by ROS generation. These results showed that and induce cancer cell death by activating autophagy signaling, which is correlated with altered cellular oxidative stress.

摘要

咖啡酸苯乙酯 (CAPE) 具有抗生素和抗癌活性。因此,我们旨在研究 CAPE 和咖啡酰胺衍生物在口腔鳞状细胞癌细胞 (OSCC) 系 SAS 和 OECM-1 中的抗癌特性和机制。使用 3-(4,5-二甲基噻唑-2-基)-2,5-二苯基四氮唑溴盐 (MTT) 试验评估 CAPE 和咖啡酰胺衍生物 (、、、、和 ) 的抗 OSCC 作用。通过流式细胞术分析细胞周期和总活性氧 (ROS) 产生。通过 Western blot 分析确定恶性表型的相对蛋白表达。结果表明,和在 SAS 细胞中比其他化合物具有更强的细胞毒性。或处理 48 h 后,细胞周期 S 期或 G2/M 期阻滞诱导,细胞内 ROS 在 24 h 时增加,然后在两种细胞系中在 48 h 时减少。细胞周期调节蛋白和抗 ROS 蛋白的表达水平下调。此外,或处理通过 ROS 生成激活的 mTOR-ULK1-P62-LC3 自噬信号抑制恶性表型。这些结果表明,和通过激活与细胞氧化应激改变相关的自噬信号诱导癌细胞死亡。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/92de/10298160/cde72bb36552/ijms-24-09819-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/92de/10298160/577949aa8cd8/ijms-24-09819-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/92de/10298160/90562bfe99f2/ijms-24-09819-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/92de/10298160/b38cf01a6e5e/ijms-24-09819-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/92de/10298160/fa7309790a04/ijms-24-09819-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/92de/10298160/cde72bb36552/ijms-24-09819-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/92de/10298160/577949aa8cd8/ijms-24-09819-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/92de/10298160/90562bfe99f2/ijms-24-09819-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/92de/10298160/b38cf01a6e5e/ijms-24-09819-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/92de/10298160/fa7309790a04/ijms-24-09819-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/92de/10298160/cde72bb36552/ijms-24-09819-g005.jpg

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