As a potential antitumor herbal medicine, plantamajoside (PMS) benefits the treatment of many human malignances. However, the role of PMS in the progression of hepatocellular carcinoma (HCC) and the related molecular mechanisms is still unknown. Here, we proved that the cell viabilities of HepG2 cells were gradually decreased with the increasing concentrations of CoCl₂ and/or PMS via cell counting kit‐8 assay. Meanwhile, 3‐(4,5‐dimethyl‐2‐thiazolyl)‐2,5‐diphenyl‐2H‐tetrazolium bromide (MTT) and western blot assays were used to further confirm that PMS inhibited the CoCl₂‐induced cell proliferation in HepG2 cells via suppressing the Ki67 and proliferating cell nuclear antigen expressions. We also performed wound‐healing and transwell assays and demonstrated that PMS inhibited CoCl₂‐induced migration and invasion in HepG2 cells via suppressing the epithelial–mesenchymal transition (EMT) process. In addition, the use of 3‐(5′‐hydroxymethyl‐2′‐furyl)‐1‐benzylindazole further proved that PMS inhibited the malignant biological behaviors of HepG2 cells under hypoxic condition by suppressing the hypoxia‐inducible factor‐1α (HIF‐1α) expression. Besides, we further confirmed that PMS suppressed the growth and metastasis of implanted tumors in vivo. Given that PMS suppressed the proliferation and EMT induced by CoCl₂ in HCC cells via downregulating HIF‐1α signaling pathway, we provided evidence that PMS might be a novel anti‐cancer drug for HCC treatment.

中文翻译：

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车前子甙可通过调节缺氧诱导因子-1α依赖性基因表达来抑制肝癌细胞的增殖和上皮向间质转化。

作为潜在的抗肿瘤草药，车前子甙（PMS）有益于治疗许多人类恶性肿瘤。然而，PMS在肝细胞癌（HCC）进程中的作用及其相关的分子机制仍是未知的。在这里，我们通过细胞计数试剂盒8分析法证明，随着CoCl ₂和/或PMS浓度的增加，HepG2细胞的细胞活性逐渐降低。同时，使用3-（4,5-二甲基-2-噻唑基）-2,5-二苯基-2H-四唑溴化物（MTT）和W​​estern印迹法进一步证实PMS抑制了Cop ₂诱导的HepG2细胞增殖。通过抑制Ki67和增殖细胞核抗原的表达。我们还进行了伤口愈合和Transwell分析，并证明了PMS抑制了CoCl₂通过抑制上皮-间质转化（EMT）过程诱导HepG2细胞迁移和侵袭。此外，使用3-（5'-羟甲基-2'-呋喃基）-1-苄基吲唑进一步证明PMS通过抑制缺氧诱导因子-1α（HIF-）抑制缺氧条件下HepG2细胞的恶性生物学行为。 1α）表达式。此外，我们进一步证实PMS抑制了体内植入肿瘤的生长和转移。鉴于PMS通过下调HIF-1α信号通路抑制了CoCl ₂在HCC细胞中的增殖和EMT ，我们提供的证据表明PMS可能是用于HCC治疗的新型抗癌药物。