工作与生活平衡的变化导致年轻人宫颈癌发病率上升。一种名为人参皂苷Rk1的次要人参皂苷可以抑制人类癌细胞的生长和存活，然而，人参皂苷Rk1是否抑制HeLa细胞增殖尚不清楚。人参皂苷Rk1以剂量依赖的方式阻断了HeLa细胞的G0/G1期，并抑制了细胞分裂和增殖。人参皂苷Rk1还通过caspase 3、PARP和caspase 6显著激活了凋亡信号通路。此外，人参皂苷Rk1增加了LC3B蛋白的表达，表明自噬信号通路得到了促进。基因本体论富集分析和京都基因与基因组百科全书（KEGG）信号通路富集分析表明内质网信号通路的蛋白质处理发生了下调作用，与实时定量PCR和Western blot检测结果一致，显示在与人参皂苷Rk1处理的HeLa细胞中，YOD1、HSPA4L、DNAJC3和HSP90AA1的表达水平明显下降，其中YOD1的下降幅度最显著。这些发现表明，人参皂苷Rk1对HeLa细胞的毒性可以通过抑制内质网中的蛋白质合成和增强细胞凋亡来解释，其中YOD1作为宫颈癌治疗的潜在靶点。 © 2023 The Korean Society of Ginseng. Publishing services by Elsevier B.V.

Changes to work-life balance has increased the incidence of cervical cancer among younger people. A minor ginseng saponin known as ginsenoside Rk1 can inhibit the growth and survival of human cancer cells; however, whether ginsenoside Rk1 inhibits HeLa cell proliferation is unknown.Ginsenoside Rk1 blocked HeLa cells in the G0/G1 phase in a dose-dependent manner and inhibited cell division and proliferation. Ginsenoside Rk1 markedly also activated the apoptotic signaling pathway via caspase 3, PARP, and caspase 6. In addition, ginsenoside Rk1 increased LC3B protein expression, indicating the promotion of the autophagy signaling pathway. Protein processing in the endoplasmic reticulum signaling pathway was downregulated in Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses, consistent with teal-time quantitative PCR and western blotting that showed YOD1, HSPA4L, DNAJC3, and HSP90AA1 expression levels were dramatically decreased in HeLa cells treated with ginsenoside Rk1, with YOD1 was the most significantly inhibited by ginsenoside Rk1 treatment.These findings indicate that the toxicity of ginsenoside Rk1 in HeLa cells can be explained by the inhibition of protein synthesis in the endoplasmic reticulum and enhanced apoptosis, with YOD1 acting as a potential target for cervical cancer treatment.© 2023 The Korean Society of Ginseng. Publishing services by Elsevier B.V.