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山东大学学报(医学版) ›› 2015, Vol. 53 ›› Issue (9): 13-18.doi: 10.6040/j.issn.1671-7554.0.2015.281

• 基础医学 • 上一篇    下一篇

氯化两面针碱对前列腺癌细胞PC-3增殖与凋亡的影响

程翔宇1, 邢锐2, 邢召全1, 郭兆新1, 郭晓宇3, 苏静3, 孟力维1, 刘照旭1,3   

  1. 1. 山东大学齐鲁医院泌尿外科, 山东 济南 250012;
    2. 临邑县人民医院泌尿外科, 山东 临邑 251500;
    3. 山东大学护理学院, 山东 济南 250012
  • 收稿日期:2015-03-16 出版日期:2015-09-10 发布日期:2015-09-10
  • 通讯作者: 刘照旭。E-mail:zhaoxvl@sdu.edu.cn E-mail:zhaoxvl@sdu.edu.cn

Effects of nitidine chloride on the proliferation and apoptosis of prostate cancer PC-3 cells

CHENG Xiangyu1, XING Rui2, XING Zhaoquan1, GUO Zhaoxin1, GUO Xiaoyu3, SU Jing3, MENG Liwei1, LIU Zhaoxu1,3   

  1. 1. Department of Urology, Qilu Hospital of Shandong University, Jinan 250012, Shandong, China;
    2. Department of Urology, Peoples Hospital of Linyi, Linyi 251500, Shandong, China;
    3. School of Nursing, Shandong University, Jinan 250012, Shandong, China
  • Received:2015-03-16 Online:2015-09-10 Published:2015-09-10
  • Contact: 刘照旭。E-mail:zhaoxvl@sdu.edu.cn E-mail:zhaoxvl@sdu.edu.cn

摘要: 目的 探讨氯化两面针碱对前列腺癌细胞PC-3增殖及凋亡的影响作用。方法 采用MTT、细胞划痕和Transwell侵袭实验评估氯化两面针碱对人前列腺癌细胞PC-3增殖与侵袭的影响;流式细胞术检测氯化两面针碱对PC-3细胞凋亡的影响;免疫印迹检测AKT/mTOR及细胞凋亡蛋白B细胞淋巴瘤基因-2相关X蛋白(Bax)和B细胞淋巴瘤基因-2(Bcl-2)的表达,应用PI3K通路抑制剂LY294002探讨抑制AKT通路对前列腺癌细胞PC-3的影响。结果 氯化两面针碱能抑制PC-3细胞的增殖与侵袭,且具有剂量依赖性(P<0.01)。氯化两面针碱可下调Bcl-2、而上调Bax的蛋白表达,Bax/Bcl-2比例明显上升(P<0.01),抑制AKT和mTOR通路的磷酸化,诱导前列腺癌细胞PC-3凋亡。联合应用LY294002发现,抑制AKT通路可增强氯化两面针碱对前列腺癌细胞PC-3增殖和侵袭的抑制作用。结论 氯化两面针碱能够抑制前列腺癌细胞PC-3的增殖与侵袭,诱导其凋亡,并通过抑制AKT/mTOR磷酸化发挥其抗前列腺癌作用,可作为一种潜在治疗前列腺癌的药物。

关键词: 氯化两面针碱, 细胞侵袭, 前列腺肿瘤, AKT/mTOR通路, 细胞凋亡

Abstract: Objective To evaluate the effects of nitidine chloride on the proliferation and apoptosis of prostate cancer cells PC-3 in vitro. Methods MTT, scratch migration and Transwell were used to examine the changes in the proliferation and invasions of human prostate cancer cell PC-3 after nitidine chloride treatment. Flow cytometry was used to examine the changes in cell apoptosis of PC-3. Immunoblot analysis was adopted to detect the expression of AKT/mTOR, Bcell-associated x protein (Bax) and Bcell lymphoma-2 (Bcl-2). A specific PI3K inhibitor, LY294002, was used to evaluate the influence of prostate cancer cells by inhibiting AKT pathway. Results Nitidine chloride inhibited the proliferation and invasion of PC-3 cells in a dose-dependent manner (P<0.01). Nitidine chloride inhibited AKT and mTOR pathways phosphorylation, accompanied by up-regulation of Bax, and down-regulation of Bcl-2. Nitidine chloride significantly increased the ratio of Bax/Bcl-2 (P<0.01), to induce prostate cancer cells apoptosis. Furthermore, combined use of LY294002 inhibited AKT pathway, which could enhance the anti-proliferation and anti-invasion effectsof nitidine chloride. Conclusion Nitidine chloride can suppress the proliferation, migration, invasion and induce the apoptosis of prostate cancer cells in vitro. Nitidine chloride also plays a role in anti-cancer via inhibiting AKT/mTOR pathway phosphorylation, which implies that nitidine chloride may be a promising therapeutic drug for prostate cancer.

Key words: Prostate neoplams, Apoptosis, Nitidine chloride, AKT /mTOR pathway, Cell metastasis

中图分类号: 

  • R737.25
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