扁塑藤素抑制卵巢癌细胞株OVCAR3生长的实验研究

Pristimerin inhibits the proliferation of ovarian cancer cell line OVCAR3

背景与目的:蛋白酶体抑制剂作为肿瘤的靶向治疗方法之一,近年来备受关注。研究发现,蛋白酶体抑制剂PS-341(bortezomib)可以诱导多种卵巢癌细胞株凋亡。扁塑藤素是一种天然化合物,具有蛋白酶体抑制剂的作用。本研究旨在研究扁塑藤素对卵巢癌细胞的增殖抑制作用。方法:采用MTT增殖抑制试验、Hoechst 33258荧光染色、Western blot检测等方法,研究扁塑藤素对卵巢癌细胞株OVCAR3增殖的抑制作用。结果:扁塑藤素可以抑制卵巢癌细胞增殖,IC_(50)值为(2.74±0.04)μmol/L;通过Hoechst 33258荧光染色、PARP蛋白裂解,证实扁塑藤素通过诱导卵巢癌细胞凋亡抑制其增殖,其作用机制是抑制了肿瘤细胞信号通路ERK及Akt磷酸化。结论:扁塑藤素通过抑制ERK和Akt磷酸化,诱导卵巢癌细胞凋亡,抑制其生长,是一个有治疗卵巢癌临床应用价值的天然药物。

Background and purpose： Recently, proteasome inhibitors have been the target for cancer therapy. It has been indicated that PS-341 （bortezomib） can induce apoptosis in many ovarian cancer lines. Pristimerin is a natural product that has the ability to inhibit proteasome. Therefore we investigated if pristimerin could inhibit the proliferation of ovarian cancer cell lines. Methods： We investigated the action ofpristimerin against the proliferation of the OVCAR3 cell line through MTT assay, Hoechst staining and Western blot. Results： Pristimerin can inhibit the proliferation of ovarian cancer at an IC50 of （2.74±0.04）μmol/L. Hoechst staining and cleavage of PARP has demonstrated that pristimerin can induce OVCAR3 cell line apoptosis. We also found that pristimerin can inhibit the phosphorylation of ERK and Akt. Conclusion： Pristimerin can inhibit the proliferation of ovarian cancer and induce apoptosis through inhibiting the phosphorylation of ERK and Akt. It is a potential natural product against ovarian cancer.