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引用本文格式: Zhao Xin-Jun,Li Xun,Wang Shu-Heng,LIJiuZhi. A physical mechanism of VPRBP protein and Abl kinase inducing and inhibiting prostate cancer [J]. J. At. Mol. Phys., 2022, 39(5): 051003 (in Chinese) [赵新军,李循,王书恒,李九智. VPRBP 蛋白与Abl 激酶诱发、抑制前列腺癌的 一种物理机制 [J]. 原子与分子物理学报, 2022, 39(5): 051003]
 
VPRBP 蛋白与Abl 激酶诱发、抑制前列腺癌的 一种物理机制
A physical mechanism of VPRBP protein and Abl kinase inducing and inhibiting prostate cancer
摘要点击 82  全文点击 12  投稿时间:2021-06-28  修订日期:2021-07-22
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DOI编号   
中文关键词   VPRBP 蛋白  Abl 激酶  前列腺癌
英文关键词   VPRBP protein  Abl kinase  prostate cancer
基金项目   国家自然科学基金
作者单位E-mail
赵新军 伊犁师范大学 zhaoxinjunzxj@163.com 
李循 新疆维吾尔自治区人民医院  
王书恒 新疆维吾尔自治区人民医院  
李九智 新疆维吾尔自治区人民医院 lijiuzhi2017@163.com 
中文摘要
    在本文基于Hill 动力学与 Michaelis-Menten 方程,建立理论模型研究 VPRBP 蛋白与 Abl 激酶诱发、抑制前列腺癌的一种物理机制。研究发现,DNA 损伤使得 ATM(共济失调毛细血管扩张症突变)很快激活,并激活上调 p53 蛋白表达,DNA 损伤的后续破坏会在很大程度上通过 p53 表达上调而被抑制。VPRBP 通过上调 MDM2 蛋白的激活水平,使得 p53 表达水平异常,进而无法正常抑制前列腺癌的发生发展。通过考察 Abl 在前列腺癌进程中的作用发现,Abl 使得 AKT 的表达水平下调,由于 Abl 对 AKT 的抑制作用,致使在 AKT 信号通路中MDM2表达水平受到抑制,进而稳定 p53 表达。由此表明了,过少的 Abl 对 AKT 的抑制程度减弱,不仅使得细胞代谢出现紊乱,而且还会促使 p53 正常的周期表达水平异常,对 DNA 损伤诱发的肿瘤抑制性减弱,进而促进前列腺癌的发生发展。基于本文模型,可以预测 VPRBP 与 Abl作为诱发、抑制前列腺癌的调节剂对现有和潜在的抗癌治疗较为敏感。VPRBP 与 Abl 在诱发、抑制前列腺癌过程中的时滞效应,导致信号通路中 p53 与 PTEN 蓄积量增多、AKT 蓄积量减少,以及 Plk1 周期振荡相位转移,可用于预测旨在阻断前列腺癌细胞周期进程的潜在治疗效果。本文结果揭示了VPRBP 与Abl 诱发、抑制前列腺癌进程的一种调控作用机制,理论结果符合实验,可为设计阻断前列腺癌的通路治疗方案提供理论依据。
英文摘要
    In this paper, based on Hill dynamics and Michaelis-Menten equation, we built a theoretical model to study a physical mechanism of VPRBP protein and Abl kinase inducing and inhibiting prostate cancer. We found that DNA damage quickly activates ATM and activates the up-regulation of p53. The subsequent damage of DNA damage will be largely inhibited by the up-regulation of p53 expression. VPRBP protein up-regulates MDM2, which makes the expression level of p53 abnormal. Thus, it is impossible to normalize the occurrence and development of prostate cancer. By investigating the role of Abl in the progression of prostate cancer, We also found that Ab1 down-regulates the expression level of AKT. Due to the inhibitory effect of Ab1 on AKT, which inhibits the expression level of MDM2 in the AKT signaling pathway, thereby stabilizing the expression of p53. This indicates that the deficient Ab1 can weaken the degree of inhibition of AKT. It not only makes cell metabolism disorder, but also promote the abnormal expression level of p53 in the normal cycle, and weaken the tumor suppression induced by DNA damage, which promote the occurrence and development of prostate cancer. Based on the model in this paper, it can be predicted that VPRBP and Abl as regulators that induce and inhibit prostate cancer are more sensitive to existing and potential anti-cancer treatments. VPRBP and Abl act as a time delay effect in the process of inducing and inhibiting prostate cancer, which result in increased accumulation of p53 and PTEN in the signal pathway, and decreased AKT, as well as Plk1 phase shift of periodic oscillations. It can used to predict the cell cycle process aimed at blocking prostate cancer cells potential therapeutic effect. The results of this paper reveal a regulatory mechanism of VPRBP protein and Abl in the process of inducing and inhibiting prostate cancer. The theoretical results are consistent with experiments and can provide a theoretical basis for the design of treatment plans that block prostate cancer.

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