Wang Yan, Liu Mingzhu, Chen Shenglan, Wu Qin
College of Medical Technology, Jiangsu Vocational College of Medicine, Yancheng, Jiangsu 224000, P.R. China.
Department of Dermatology, Nanjing Integrated Traditional Chinese and Western Medicine Hospital Affiliated to Nanjing University of Chinese Medicine, Nanjing, Jiangsu 210014, P.R. China.
Exp Ther Med. 2020 Mar;19(3):2296-2302. doi: 10.3892/etm.2020.8442. Epub 2020 Jan 10.
Plantamajoside (PMS) has been shown to have anticancer effects and is the main compound of . The aim of the present study was to investigate the effects of PMS on malignant melanoma and its molecular mechanisms. The malignant melanoma cell line A2058 was treated with different concentrations of PMS (0, 20, 80 and 160 µg/ml) for 24, 48 or 72 h, followed by cell viability detection using the Cell Counting Kit-8 assay. The present results suggested that PMS inhibited cell viability in a dose-dependent manner. In addition, flow cytometry was used to analyze cell apoptosis, and Transwell assays were used to investigate cell migration and invasion. The present results suggested that PMS induced A2058 cell apoptosis, and inhibited cell invasion and migration in a dose-dependent manner. In order to study the molecular mechanism by which PMS inhibited malignant melanoma growth and metastasis, reverse transcription-quantitative PCR and western blotting were used to determine the expression levels of apoptotic-related genes and PI3K/AKT signaling pathway-related proteins. The present results indicated that PMS inhibited the protein and mRNA expression of , and promoted the expression of Bax and caspase-3 in a dose-dependent manner. The protein expression level of phosphorylated-AKT was dose-dependently reduced by PMS treatment. Collectively, the present results suggested that PMS inhibited the invasion, migration and viability of malignant melanoma cells. In addition, PMS induced apoptosis by regulating the expression levels of apoptotic-related genes and the activation of the PI3K/AKT signaling pathway, thereby exerting anti-malignant melanoma effects.
连翘酯苷（PMS）已被证明具有抗癌作用，是……的主要化合物。本研究的目的是探讨PMS对恶性黑色素瘤的影响及其分子机制。将恶性黑色素瘤细胞系A2058分别用不同浓度的PMS（0、20、80和160µg/ml）处理24、48或72小时，然后使用细胞计数试剂盒-8检测法检测细胞活力。目前的结果表明，PMS以剂量依赖的方式抑制细胞活力。此外，采用流式细胞术分析细胞凋亡，采用Transwell实验研究细胞迁移和侵袭。目前的结果表明，PMS诱导A2058细胞凋亡，并以剂量依赖的方式抑制细胞侵袭和迁移。为了研究PMS抑制恶性黑色素瘤生长和转移的分子机制，采用逆转录定量PCR和蛋白质印迹法检测凋亡相关基因和PI3K/AKT信号通路相关蛋白的表达水平。目前的结果表明，PMS抑制……的蛋白质和mRNA表达，并以剂量依赖的方式促进Bax和caspase-3的表达。PMS处理可使磷酸化-AKT的蛋白质表达水平呈剂量依赖性降低。总体而言，目前的结果表明，PMS抑制恶性黑色素瘤细胞的侵袭、迁移和活力。此外，PMS通过调节凋亡相关基因的表达水平和激活PI3K/AKT信号通路诱导细胞凋亡，从而发挥抗恶性黑色素瘤的作用。
