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Baohuoside I Inhibits the Proliferation of Pancreatic Cancer Cells via mTOR/S6K1-Caspases/Bcl2/Bax Apoptotic Signaling.
Cancer Management and Research ( IF 2.5 ) Pub Date : 2019-12-19 , DOI: 10.2147/cmar.s228926
Fubiao Ni 1 , Hengjie Tang 1 , Cheng Wang 1 , Hewei Zhang 1 , Chenlei Zheng 1 , Ning Zhang 2 , Bicheng Chen 1 , Linxiao Sun 1
Affiliation  

BACKGROUND Although the incidence of pancreatic cancer has increased markedly, the 5-year survival rate for this disease is considerably low compared with other types of cancer. Moreover, the mortality rate of pancreatic cancer is similar to its incidence rate. Current therapeutic agents exhibit a lack of specificity for pancreatic cancer. Baohuoside I is traditionally used to treat orgasmic disorder and inflammation. However, its role in pancreatic cancer is unknown. OBJECTIVE To explore the effects of Baohuoside I on pancreatic cancer and to study the potential-related molecular mechanism. MATERIALS AND METHODS In the present study, the antineoplastic effect of Baohuoside I was investigated with regard to pancreatic cancer via colony formation, transwell and migration assay. The energy metabolism changes of pancreatic cancer were tested by flow cytometry analysis and oxidative phosphorylation and glycolysis assay. The target signaling members were analyzed by Western blot. RESULTS Baohuoside I inhibited the cell growth of pancreatic cancer cells. In addition, it affected intracellular energy metabolism to induce cancer cell apoptosis via the mTOR/S6K1 and the caspase/Bcl2/Bax signaling pathways. CONCLUSION The present data provide further insight into the development of novel drugs against pancreatic cancer.

中文翻译:

Baohuoside I 通过 mTOR/S6K1-Caspases/Bcl2/Bax 凋亡信号通路抑制胰腺癌细胞的增殖。

背景尽管胰腺癌的发病率显着增加,但与其他类型的癌症相比,这种疾病的 5 年生存率相当低。此外,胰腺癌的死亡率与其发病率相似。目前的治疗剂对胰腺癌缺乏特异性。Baohuside I 传统上用于治疗性高潮障碍和炎症。然而,它在胰腺癌中的作用尚不清楚。目的探讨保活苷Ⅰ对胰腺癌的作用,并探讨其潜在相关分子机制。材料与方法 在本研究中,通过集落形成、transwell 和迁移试验研究了宝霍苷 I 对胰腺癌的抗肿瘤作用。通过流式细胞仪分析和氧化磷酸化和糖酵解测定法检测胰腺癌的能量代谢变化。通过蛋白质印迹分析靶信号成员。结果宝霍苷Ⅰ对胰腺癌细胞的生长有抑制作用。此外,它通过mTOR/S6K1和caspase/Bcl2/Bax信号通路影响细胞内能量代谢诱导癌细胞凋亡。结论 目前的数据为开发抗胰腺癌的新药提供了进一步的见解。它通过mTOR/S6K1和caspase/Bcl2/Bax信号通路影响细胞内能量代谢诱导癌细胞凋亡。结论 目前的数据为开发抗胰腺癌的新药提供了进一步的见解。它通过mTOR/S6K1和caspase/Bcl2/Bax信号通路影响细胞内能量代谢诱导癌细胞凋亡。结论 目前的数据为开发抗胰腺癌的新药提供了进一步的见解。
更新日期:2019-12-19
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