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蜂毒通过诱导细胞周期停滞和凋亡并抑制细胞迁移来预防胰腺癌。

Bee venom protects against pancreatic cancer via inducing cell cycle arrest and apoptosis with suppression of cell migration.

作者信息

Zhao Jing, Hu Weiguo, Zhang Zejia, Zhou Zegao, Duan Jiayue, Dong Zheng, Liu Hao, Yan Changqing

机构信息

Department of General Surgery, The Second Hospital of Hebei Medical University, Shijiazhuang, China.

North China Pharmaceutical Co., Ltd., Shijiazhuang, China.

出版信息

J Gastrointest Oncol. 2022 Apr;13(2):847-858. doi: 10.21037/jgo-22-222.

DOI:10.21037/jgo-22-222
PMID:35557571
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9086033/
Abstract

BACKGROUND

Pancreatic cancer seriously threatens human health. Bee venom is a mixture of enzymes, peptides, and amines. Due to its biological activity, bee venom is widely used as an anti-inflammatory agent and pain reliever. However, little is known about the effect of bee venom on pancreatic cancer.

METHODS

Firstly, the Cell Counting Kit-8 (CCK-8) assay was conducted to analyze the cytotoxicity of bee venom on PANC-1 and AsPC-1 cells. Then, we evaluated the cell cycle and apoptosis by flow cytometry and the terminal deoxynucleotidyl transferase (TdT) dUTP Nick-End Labeling (TUNEL) assay. In addition, cell migration was analyzed by the cell scratch test and Transwell assay. Western blot was performed to assess the expression of proteins involved in the regulation of cell cycle arrest and apoptosis.

RESULTS

Results demonstrated that bee venom significantly suppressed cell proliferation via inducing cell cycle arrest and apoptosis with suppression of cell migration. Bee venom induced S phase arrest and ameliorated the protein expression of cyclins and cyclin-dependent kinases (CDKs). At the same time, bee venom can activate the p53-p21 pathway. Experimental data also showed that bee venom induced cell apoptosis and impeded cell migration.

CONCLUSIONS

The present study revealed that bee venom could effectively inhibit tumor progression in pancreatic cancer cells, indicating the possibility of bee venom as an anti-tumor drug in pancreatic cancer.

摘要

背景

胰腺癌严重威胁人类健康。蜂毒是酶、肽和胺的混合物。由于其生物活性,蜂毒被广泛用作抗炎剂和止痛剂。然而,关于蜂毒对胰腺癌的影响知之甚少。

方法

首先,进行细胞计数试剂盒-8(CCK-8)检测以分析蜂毒对PANC-1和AsPC-1细胞的细胞毒性。然后,我们通过流式细胞术和末端脱氧核苷酸转移酶(TdT)介导的dUTP缺口末端标记(TUNEL)检测评估细胞周期和细胞凋亡。此外,通过细胞划痕试验和Transwell检测分析细胞迁移。进行蛋白质印迹法以评估参与细胞周期阻滞和细胞凋亡调节的蛋白质的表达。

结果

结果表明,蜂毒通过诱导细胞周期阻滞和细胞凋亡以及抑制细胞迁移来显著抑制细胞增殖。蜂毒诱导S期阻滞并改善细胞周期蛋白和细胞周期蛋白依赖性激酶(CDK)的蛋白质表达。同时,蜂毒可激活p53-p21通路。实验数据还表明,蜂毒诱导细胞凋亡并阻碍细胞迁移。

结论

本研究表明,蜂毒可有效抑制胰腺癌细胞的肿瘤进展,表明蜂毒作为胰腺癌抗肿瘤药物的可能性。

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