Van Hung Hoang, Kieu Oanh Nguyen Thi, Nguyen Phu Hung, Le Thi Thanh Huong, Hoang Viet
Thai Nguyen University, Tan Thinh Ward, Thai Nguyen City, Vietnam.
University of Science and Technology of Hanoi, Vietnam Academy of Science and Technology, 18 Hoang Quoc Viet, Cau Giay, Ha Noi, Vietnam.
J Appl Biomed. 2025 Mar;23(1):12-25. doi: 10.32725/jab.2025.002. Epub 2025 Mar 21.
This study aimed to investigate the phytochemical composition of Psychotria montana extract (PME) and evaluate its inhibitory effects on MCF7 breast cancer cells.
The chemical composition of PME was analyzed using UPLC-QToF-MS. The effects of PME on cell proliferation were evaluated using the MTT assay. Flow cytometry was used for cell cycle and apoptosis analysis. The effects of PME on the transcription of cell cycle control genes were assessed using real-time PCR.
UPLC-QToF-MS analysis revealed major compounds of PME, including terpenoids and flavonoids, with the potential to inhibit proliferation, migration, and induce apoptosis in MCF7 cancer cells. PME effectively suppressed MCF7 cell proliferation under 2D culture, with a low IC50 value of 34.7 µg/ml. PME also hindered cell migration (p < 0.01) and reduced spheroid number (p < 0.001) and size (p < 0.001) in serum-free 3D culture. Apoptosis analysis via nuclear staining with DAPI and flow cytometry revealed an increase in the number of apoptotic cells after PME treatment (p < 0.001). Additionally, the PME induced cell cycle arrest at the G0/G1 phase (p < 0.05). PME altered the expression of cell cycle control genes (cyclins and CDKs) as well as cancer suppressor genes including p16, p27, and p53 at the transcriptional level (mRNA). The results of molecular docking suggest that the compounds present in PME exhibit a high binding affinity for CDK3, CDK4, CDK6, and CDK8 proteins, which are essential regulators of the cell cycle.
Psychotria montana has the potential to inhibit cancer cells by inducing apoptosis and halting the cell cycle of MCF7 breast cancer cells.
本研究旨在调查山地九节提取物（PME）的植物化学成分，并评估其对MCF7乳腺癌细胞的抑制作用。
使用超高效液相色谱-四极杆飞行时间质谱联用仪（UPLC-QToF-MS）分析PME的化学成分。采用MTT法评估PME对细胞增殖的影响。流式细胞术用于细胞周期和凋亡分析。使用实时聚合酶链反应（PCR）评估PME对细胞周期控制基因转录的影响。
UPLC-QToF-MS分析揭示了PME的主要化合物，包括萜类化合物和黄酮类化合物，它们具有抑制MCF7癌细胞增殖、迁移和诱导凋亡的潜力。在二维培养条件下，PME能有效抑制MCF7细胞增殖，半数抑制浓度（IC50）值低至34.7μg/ml。在无血清三维培养中，PME还阻碍细胞迁移（p<0.01），并减少球体数量（p<0.001）和大小（p<0.001）。通过4',6-二脒基-2-苯基吲哚（DAPI）核染色和流式细胞术进行的凋亡分析显示，PME处理后凋亡细胞数量增加（p<0.001）。此外，PME诱导细胞周期停滞在G0/G1期（p<0.05）。PME在转录水平（mRNA）改变了细胞周期控制基因（细胞周期蛋白和细胞周期蛋白依赖性激酶）以及包括p16、p27和p53在内的抑癌基因的表达。分子对接结果表明，PME中存在的化合物对细胞周期的关键调节因子细胞周期蛋白依赖性激酶3（CDK3）、细胞周期蛋白依赖性激酶4（CDK4）、细胞周期蛋白依赖性激酶6（CDK6）和细胞周期蛋白依赖性激酶8（CDK8）蛋白表现出高结合亲和力。
山地九节有潜力通过诱导凋亡和阻止MCF7乳腺癌细胞的细胞周期来抑制癌细胞。
