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[布索喷丁(BP5)的抗肿瘤机制]

[Antitumor mechanism of Bursopentin (BP5)].

作者信息

Guo Xiangling, Wang Chen, Li Xiaokang, Wu Tingcai, Li Deyuan, Chen Puyan

出版信息

Wei Sheng Wu Xue Bao. 2015 Feb 4;55(2):235-45.

PMID:25958705
Abstract

OBJECTIVE

Bursopentin (BP5) is a multi-functional bioactive peptide with functions of immunomodulatory, antioxidant and antitumor. However, the antitumor mechanism of BP5 is still unclear.

METHODS

We constructed T7 phage cDNA library of DT40 cells, and the proteins interacted with BP5 were identified. Then, the expression profile of BP5-treated DT40 cells were analyzed using gene microarray, p53 Luciferase activity was detected.

RESULTS

The results of the expression profiling revealed that BP5 regulated expression of 1078 genes, of which 537 were up-regulated and 541 were down-regulated. Differentially expressed genes involved in various pathways were identified, of which 25 pathways were associated with immune responses and tumorigenic processes, including the p53 signaling. Furththmore, BP5 significantly enhanced p53 luciferase activity and stimulated expression of p53 protein in HCT116 cells.

CONCLUSION

These results suggest that BP5 exerted antitumor activity through p53 signaling and that this study provides novel insights on the antitumor mechanism of BP5.

摘要

目的

布索喷丁(BP5)是一种具有免疫调节、抗氧化和抗肿瘤功能的多功能生物活性肽。然而,BP5的抗肿瘤机制仍不清楚。

方法

构建DT40细胞的T7噬菌体cDNA文库,并鉴定与BP5相互作用的蛋白质。然后,使用基因芯片分析BP5处理的DT40细胞的表达谱,检测p53荧光素酶活性。

结果

表达谱分析结果显示,BP5调节1078个基因的表达,其中537个上调,541个下调。鉴定了参与各种途径的差异表达基因,其中25条途径与免疫反应和肿瘤发生过程相关,包括p53信号通路。此外,BP5显著增强HCT116细胞中的p53荧光素酶活性并刺激p53蛋白的表达。

结论

这些结果表明,BP5通过p53信号通路发挥抗肿瘤活性,本研究为BP5的抗肿瘤机制提供了新的见解。

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[Antitumor mechanism of Bursopentin (BP5)].[布索喷丁(BP5)的抗肿瘤机制]
Wei Sheng Wu Xue Bao. 2015 Feb 4;55(2):235-45.
2
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引用本文的文献

1
Bursopentin (BP5) induces G1 phase cell cycle arrest and endoplasmic reticulum stress/mitochondria-mediated caspase-dependent apoptosis in human colon cancer HCT116 cells.布索喷丁(BP5)可诱导人结肠癌HCT116细胞发生G1期细胞周期阻滞以及内质网应激/线粒体介导的半胱天冬酶依赖性凋亡。
Cancer Cell Int. 2019 May 16;19:130. doi: 10.1186/s12935-019-0849-3. eCollection 2019.