Department of Breast Surgery, The Affiliated Zhongshan Hospital of Xiamen University, Xiamen, Fujian P. R. of China.
Department of Breast Surgery, The First Affiliated Hospital of Xiamen University Xiamen, Fujian, P. R. of China.
Acta Pharm. 2023 Jan 24;73(1):75-90. doi: 10.2478/acph-2023-0005. Print 2023 Mar 1.
Breast cancer is one of the most common malignant tumors in women and it is the most frequently diagnosed cancer in the world. Ampelopsin (AMP) is a purified component from the root of . It is reported that AMP could significantly inhibit the proliferation of breast cancer cells. However, the antitumor mechanism against breast cancer has not yet been fully elucidated. The purpose of this work was to study the role of AMP against breast cancer MDA-MB-231 cells and to further investigate the underlying mechanism. PI3K/AKT/mTOR plays a very important role in tumor cell growth and proliferation and we hypothesize that AMP may inhibit this pathway. In the present work, the results showed that AMP could significantly inhibit the growth of breast cancer MDA-MB-231 cells and . In addition, treatment with AMP decreased the levels of PI3K, AKT and mTOR, as well as cyclin B1 expression, followed by p53/p21 pathway activation to arrest the cell cycle at G2/M. Moreover, it demonstrated a positive association between cyclin B1 and PI3K/AKT/mTOR levels. Importantly, this pathway was found to be regulated by cyclin B1 in MDA-MB-231 cells treated with AMP. Also, it was observed that cyclin B1 overexpression attenuated cell apoptosis and weakened the inhibitory effects of AMP on cell proliferation. Together, AMP could inhibit breast cancer MDA-MB-231 cell proliferation and , due to cell cycle arrest at G2/M by inactivating PI3K/AKT/mTOR pathway regulated by cyclin B1.
乳腺癌是女性最常见的恶性肿瘤之一，也是世界上最常见的癌症。蛇葡萄素（AMP）是从葡萄科蛇葡萄属植物中提取的一种纯化成分。有报道称 AMP 可显著抑制乳腺癌细胞的增殖。然而，其针对乳腺癌的抗肿瘤机制尚未完全阐明。本研究旨在探讨 AMP 对乳腺癌 MDA-MB-231 细胞的作用及其潜在机制。PI3K/AKT/mTOR 在肿瘤细胞生长和增殖中起着非常重要的作用，我们假设 AMP 可能抑制该通路。本研究结果表明，AMP 可显著抑制乳腺癌 MDA-MB-231 细胞的生长。此外，AMP 处理降低了 PI3K、AKT 和 mTOR 的水平以及 cyclin B1 的表达，随后激活 p53/p21 通路使细胞周期阻滞在 G2/M 期。而且，cyclin B1 与 PI3K/AKT/mTOR 水平之间存在正相关。重要的是，在 AMP 处理的 MDA-MB-231 细胞中，该通路被 cyclin B1 调控。此外，观察到 cyclin B1 过表达可减弱细胞凋亡，并削弱 AMP 对细胞增殖的抑制作用。综上所述，AMP 可通过抑制 PI3K/AKT/mTOR 通路（该通路由 cyclin B1 调控）诱导乳腺癌 MDA-MB-231 细胞周期阻滞于 G2/M 期，从而抑制细胞增殖。
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