安石榴苷通过调节细胞增殖、凋亡和侵袭对人结肠癌细胞具有细胞毒性。
Punicalagin is cytotoxic to human colon cancer cells by modulating cell proliferation, apoptosis, and invasion.
发表日期:2023
作者:
Ding-Ping Sun, Hsuan-Yi Huang, Chia-Lin Chou, Li-Chin Cheng, Wen-Ching Wang, Yu-Feng Tian, Chia-Lang Fang, Kai-Yuan Lin
来源:
Cell Death & Disease
摘要:
目的:本研究的目的是探讨安石榴苷(从石榴中分离出的一种丰富的生物活性单宁化合物)对 HCT 116、HT-29 和 LoVo 三种结肠癌细胞系的抗癌作用。研究设计:正常细胞和结肠癌细胞在不同时期用不同浓度的安石榴苷处理。数据收集和分析:用CCK-8测定法测量细胞活力。使用膜联蛋白 V 和细胞死亡试剂盒以及细胞侵袭分析试剂盒对程序性细胞死亡和侵袭进行分析。 Western blot检测活性caspase-3、MMP-2、MMP-9、Snail、Slug的表达。结果:细胞活力分析结果显示,安石榴苷对结肠癌细胞具有细胞毒性,但对结肠癌细胞无细胞毒性。正常细胞以剂量和时间依赖性方式。此外,安石榴苷诱导结肠癌细胞凋亡(通过早期和晚期凋亡的结直肠癌细胞的累积百分比显示)。研究发现,安石榴苷治疗后 caspase-3 活性增加。蛋白质印迹结果还表明安石榴苷增加了活化的 caspase-3 的表达。相反,安石榴苷抑制结肠癌细胞的侵袭。此外,用安石榴苷处理结肠癌细胞可抑制 MMP-2、MMP-9、Snail 和 Slug 的表达。结论:这些结果表明,安石榴苷对结肠癌细胞的作用涉及caspase-3的激活以及MMP-2、MMP-9、Snail和Slug的抑制。
Purpose: The purpose of this study was to explore the anticancer effect of punicalagin, an abundant bioactive tannin compound isolated from Punica granatum L., on three colon cancer cell lines, namely, HCT 116, HT-29, and LoVo.Research Design: Normal and colon cancer cells were treated with different concentrations of punicalagin for different periods. Data Collection and Analysis: Cell viability was measured with a CCK-8 assay. Programmed cell death and invasion were analyzed using an annexin V and cell death kit and a cell invasion analysis kit. The expression of active caspase-3, MMP-2, MMP-9, Snail, and Slug were measured by Western blot.Results: The results of the cell viability analysis showed that punicalagin was cytotoxic to colon cancer cells, but it was not to normal cells in a dose- and time-dependent manner. Additionally, punicalagin induced apoptosis in colon cancer cells (shown by the cumulative percentage of colorectal cancer cells in early and late apoptosis). It was found that caspase-3 activity increased following punicalagin treatment. Western blot results also showed that punicalagin increased the expression of activated caspase-3. In contrast, punicalagin inhibited the invasion of colon cancer cells. Further, treatment of colon cancer cells with punicalagin suppressed the expression of MMP-2, MMP-9, Snail, and Slug. Conclusions: These results showed that the activation of caspase-3 and the inhibition of MMP-2, MMP-9, Snail and Slug were involved in the effects of punicalagin on colon cancer cells.