The potential of apigenin (APG) to enhance cisplatin’s (CDDP) chemotherapeutic efficacy was investigated in HepG2, Hep3B, and Huh7 liver cancer cell lines. The presence of 20 μM APG sensitized all cell lines to CDDP treatment (degree of sensitization based on the MTT assay: HepG2>Huh7>Hep3B). As reflected by sister chromatid exchange levels, the degree of genetic instability as well as DNA repair by homologous recombination differed among cell lines. CDDP and 20 μM APG cotreatment exhibited a synergistic genotoxic effect on Hep3B cells and a less than additive effect on HepG2 and Huh7 cells. Cell cycle delays were noticed during the first mitotic division in Hep3B and Huh7 cells and the second mitotic division in HepG2 cells. CDDP and CDDP + APG treatments reduced the clonogenic capacity of all cell lines; however, there was a discordance in drug sensitivity compared with the MMT assay. Furthermore, a senescence-like phenotype was induced, especially in Hep3B and Huh7 cells. Unlike CDDP monotherapy, the combined treatment exhibited a significant anti-invasive and anti-migratory action in all cancer cell lines. The fact that the three liver cancer cell lines responded differently, yet positively, to CDDP + APG cotreatment could be attributed to variations they present in gene expression. Complex mechanisms seem to influence cellular responses and cell fate.

在 HepG2、Hep3B 和 Huh7 肝癌细胞系中研究了芹菜素 (APG) 增强顺铂 (CDDP) 化疗功效的潜力。20 μM APG 的存在使所有细胞系对 CDDP 处理敏感（基于 MTT 测定的敏化程度：HepG2>Huh7>Hep3B）。正如姐妹染色单体交换水平所反映的那样，遗传不稳定性的程度以及通过同源重组进行的 DNA 修复在细胞系之间是不同的。CDDP 和 20 μM APG 共处理对 Hep3B 细胞显示出协同的基因毒性作用，对 HepG2 和 Huh7 细胞显示出小于累加作用。在 Hep3B 和 Huh7 细胞的第一次有丝分裂和 HepG2 细胞的第二次有丝分裂期间注意到细胞周期延迟。CDDP 和 CDDP + APG 处理降低了所有细胞系的克隆能力；然而，与 MMT 检测相比，药物敏感性存在不一致。此外，诱导了衰老样表型，尤其是在 Hep3B 和 Huh7 细胞中。与 CDDP 单一疗法不同，联合疗法在所有癌细胞系中都表现出显着的抗侵袭和抗迁移作用。三种肝癌细胞系对 CDDP + APG 共治疗的反应不同但积极，这一事实可归因于它们在基因表达中存在的变化。复杂的机制似乎影响细胞反应和细胞命运。三种肝癌细胞系对 CDDP + APG 共治疗的反应不同但积极，这一事实可归因于它们在基因表达中存在的变化。复杂的机制似乎影响细胞反应和细胞命运。三种肝癌细胞系对 CDDP + APG 共治疗的反应不同但积极，这一事实可归因于它们在基因表达中存在的变化。复杂的机制似乎影响细胞反应和细胞命运。