蟾毒灵通过 EGFR 通路抑制卵巢癌细胞增殖。
Bufalin suppresses ovarian cancer cell proliferation via EGFR pathway.
机构信息
Department of Gynecology, The First Affiliated Hospital of China Medical University, Shenyang, Liaoning 110001, China.
First Laboratory of Cancer Institute, The First Affiliated Hospital of China Medical University, Shenyang, Liaoning 110001, China.
出版信息
Chin Med J (Engl). 2021 Dec 22;135(4):456-461. doi: 10.1097/CM9.0000000000001879.
BACKGROUND
Previous studies have shown that bufalin exerts antitumor effects through various mechanisms. This study aimed to determine the antineoplastic mechanism of bufalin, an extract of traditional Chinese medicine toad venom, in ovarian cancer.
METHODS
The 3-(4,5-Dimethyl-2-thiazolyl)-2,5-diphenyl tetrazolium bromide (MTT), 5-ethynyl-2'-deoxyuridine (EdU), and colony formation assays were used to investigate the antiproliferative effect of bufalin on the ovarian cancer cell line SK-OV-3. Molecular docking was used to investigate the combination of bufalin and epidermal growth factor receptor (EGFR) protein. Western blotting was performed to detect the expression of EGFR protein and its downstream targets.
RESULTS
Bufalin inhibited the proliferation of SK-OV-3 cells in a dose- and time-dependent manner. Bufalin was confirmed to combine with EGFR protein using molecular docking and downregulate expression of EGFR. Bufalin inhibited phosphorylation of EGFR, protein kinase B (AKT), and extracellular signal-regulated kinase (ERK).
CONCLUSION
Bufalin suppresses the proliferation of ovarian cancer cells through the EGFR/AKT/ERK signaling pathway.
背景
先前的研究表明，蟾毒灵通过多种机制发挥抗肿瘤作用。本研究旨在确定蟾毒灵（一种传统中药蟾蜍毒液提取物）在卵巢癌中的抗肿瘤机制。
方法
采用 3-(4,5-二甲基-2-噻唑基)-2,5-二苯基四氮唑溴盐（MTT）、5-乙炔基-2'-脱氧尿苷（EdU）和集落形成实验来研究蟾毒灵对卵巢癌细胞系 SK-OV-3 的抗增殖作用。分子对接用于研究蟾毒灵与表皮生长因子受体（EGFR）蛋白的结合。采用 Western blot 检测 EGFR 蛋白及其下游靶标的表达。
结果
蟾毒灵呈剂量和时间依赖性地抑制 SK-OV-3 细胞的增殖。分子对接证实蟾毒灵与 EGFR 蛋白结合，并下调 EGFR 表达。蟾毒灵抑制 EGFR、蛋白激酶 B（AKT）和细胞外信号调节激酶（ERK）的磷酸化。
结论
蟾毒灵通过 EGFR/AKT/ERK 信号通路抑制卵巢癌细胞的增殖。
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