Dziedzic Arkadiusz, Kubina Robert, Kabała-Dzik Agata, Tanasiewicz Marta
Department of Conservative Dentistry with Endodontics, School of Medicine with the Division of Dentistry, Medical University of Silesia in Katowice, Pl. Akademicki 17, 41-902 Bytom, Poland.
Department of Pathology, School of Pharmacy and Division of Laboratory Medicine in Sosnowiec, Medical University of Silesia in Katowice, ul. Ostrogórska 30, 41-200 Sosnowiec, Poland.
Evid Based Complement Alternat Med. 2017;2017:6793456. doi: 10.1155/2017/6793456. Epub 2017 Jan 12.
Natural polyphenols have been observed to possess antiproliferative properties. The effects, including apoptotic potential of bioactive phenolic compounds, caffeic acid (CA) and its derivative caffeic acid phenethyl ester (CAPE), on cell proliferation and apoptosis in human head and neck squamous carcinoma cells (HNSCC) line (Detroit 562) were investigated and compared. Cancer cells apoptosis rates and cell cycle arrests were analysed by flow cytometry. Exposure to CA and CAPE was found to result in a dose-dependent decrease in the viability of Detroit 562 cells at different levels. CA/CAPE treatment did significantly affect the viability of Detroit 562 cells (MTT results). CAPE-mediated loss of viability occurred at lower doses and was more pronounced, with the concentrations which inhibit the growth of cells by 50% estimated at 201.43 M (CA) and 83.25 M (CAPE). Dead Cell Assay with Annexin V labelling demonstrated that CA and CAPE treatment of Detroit 562 cells resulted in an induction of apoptosis at 50 M and 100 M doses. The rise of mainly late apoptosis was observed for 100 M dose and CA/CAPE treatment did affect the distribution of cells in G0/G1 phase. A combination of different phenolic compounds, potentially with chemotherapeutics, could be considered as an anticancer drug.
已观察到天然多酚具有抗增殖特性。研究并比较了生物活性酚类化合物咖啡酸（CA）及其衍生物咖啡酸苯乙酯（CAPE）对人头颈部鳞状细胞癌细胞系（底特律562）的细胞增殖和凋亡的影响，包括凋亡潜力。通过流式细胞术分析癌细胞凋亡率和细胞周期阻滞情况。发现暴露于CA和CAPE会导致底特律562细胞在不同水平上的活力呈剂量依赖性下降。CA/CAPE处理确实显著影响了底特律562细胞的活力（MTT结果）。CAPE介导的活力丧失在较低剂量下发生且更为明显，抑制细胞生长50%的浓度估计为201.43μM（CA）和83.25μM（CAPE）。用膜联蛋白V标记的死细胞检测表明，CA和CAPE处理底特律562细胞在50μM和100μM剂量下导致凋亡诱导。观察到100μM剂量主要导致晚期凋亡增加，且CA/CAPE处理确实影响细胞在G0/G1期的分布。不同酚类化合物与潜在化疗药物的组合可被视为一种抗癌药物。
