Li Chujie, Wang Yue, Liang Jian, Haenen Guido R M M, Chen Yonger, Li Zhengwen, Zhang Ming, Dubois Ludwig J
Department of Pharmacology and Personalized Medicine, Research Institute for Nutrition and Translational Research in Metabolism (NUTRIM), Faculty of Health, Medicine and Life Sciences, Maastricht University, 6200MD Maastricht, The Netherlands.
The M-Lab, Department of Precision Medicine, GROW-Research Institute for Oncology and Reproduction, Maastricht University, 6200MD Maastricht, The Netherlands.
Curr Issues Mol Biol. 2025 Jan 9;47(1):36. doi: 10.3390/cimb47010036.
BACKGROUND/AIM: Flavonoids are a group of polyphenols, abundantly present in our diet. Although, based on their chemoprotective effects, intake of flavonoids is associated with a high anticancer potential as evidenced in in vitro and in vivo models, the molecular mechanism is still elusive. This study explores the antiproliferative and cytotoxic effects of the semi-synthetic flavonoid MonoHER (7-mono-O-(β-hydroxyethyl)-rutoside) in vitro on cancer cells.
HepG2 liver, MCF7 breast, and H1299 lung cancer cells were grown under ambient conditions with or without MonoHER exposure. CCK8 assay was used to assess cell viability. Apoptosis, JC-1, and mitochondrial mass were determined using flow cytometry and confocal analysis. The effects of monoHER on apoptosis proteins were detected by confocal microscopy analysis and Western blot.
It was found that MonoHER can reduce HepG2 cells' and MCF7 cells' viability, but not H1299 cells', and induced apoptosis only in HepG2 cells. MonoHER has the potential to enhance the expression of caspase-9 and caspase-3, to damage mitochondria, and to provoke the release of cytochrome C from the mitochondria.
MonoHER can inhibit cell growth and induce apoptosis especially in HepG2 human liver cancer cells by triggering the mitochondrial signal transduction pathway, leading to the release of cytochrome C in the cytoplasm and the subsequent activation of caspase-9 and caspase-3. Future research should further explore MonoHER's mechanism of action, efficacy, and potential for clinical translation.
背景/目的：黄酮类化合物是一类多酚，在我们的饮食中大量存在。尽管基于其化学保护作用，黄酮类化合物的摄入与较高的抗癌潜力相关，这在体外和体内模型中都有证据，但分子机制仍不清楚。本研究探讨了半合成黄酮类化合物单氢杨梅素（7-单-O-(β-羟乙基)-芦丁糖苷）在体外对癌细胞的抗增殖和细胞毒性作用。
将肝癌HepG2细胞、乳腺癌MCF7细胞和肺癌H1299细胞在环境条件下培养，分别给予或不给予单氢杨梅素处理。采用CCK8法评估细胞活力。使用流式细胞术和共聚焦分析测定细胞凋亡、JC-1和线粒体质量。通过共聚焦显微镜分析和蛋白质免疫印迹法检测单氢杨梅素对凋亡蛋白的影响。
发现单氢杨梅素可降低HepG2细胞和MCF7细胞的活力，但对H1299细胞无此作用，且仅能诱导HepG2细胞凋亡。单氢杨梅素有可能增强半胱天冬酶-9和半胱天冬酶-3的表达，损伤线粒体，并促使细胞色素C从线粒体释放。
单氢杨梅素可通过触发线粒体信号转导途径抑制细胞生长并诱导凋亡，尤其是在人肝癌HepG2细胞中，导致细胞质中细胞色素C的释放以及随后半胱天冬酶-9和半胱天冬酶-3的激活。未来的研究应进一步探索单氢杨梅素的作用机制、疗效及临床转化潜力。
