二甲双胍改变癌变范式中信号诱导的串扰和稳态“癌症起源的认识论”

4open Pub Date : 2019-01-01 DOI:10.1051/FOPEN/2019006
B. Brücher, I. Jamall
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引用次数: 0

摘要

降糖药物二甲双胍(Metformin)对治疗早期糖尿病有效,并与癌症发病率降低37%有关。虽然二甲双胍抗癌作用的确切机制仍有待阐明,但这篇综述显示,二甲双胍在阻断信号和串扰、抗炎和恢复体内平衡方面的多重作用,这些作用加在一起,超出了其众所周知的抗高血糖作用,这是其用于2型糖尿病的基础。二甲双胍不仅仅是一种只会一招的小马。最近发现的几种受二甲双胍影响的信号通路似乎在癌症治疗中具有潜在的价值。根据我们目前所知道的,二甲双胍促进有益作用归因于其抗炎和抗纤维化作用,主要是在体外证明的。二甲双胍激活或上调细胞周期阻滞和细胞凋亡伴随氧化应激的多种信号通路,同时抑制或下调这些信号通路,这些信号通路符合致癌的6步序列。此外,在实验室动物和癌症患者的体内研究开始解决抗癌作用的大小,并描绘其抗癌作用。在这种情况下,先前的胰腺癌和非胰腺癌试验的结果,其中包含了相当大比例的接受二甲双胍治疗的患者群体,必须根据观察到的抗癌作用重新检查,以获得更多的见解。在“癌变范式癌症起源知识论中信号稳态破坏引起的串扰”的背景下对二甲双胍的详细探索可以为了解其抗增殖机制提供有益的见解,并可能在未来的抗癌治疗中发挥相关作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Metformin alters signaling induced crosstalk and homeostasis in the carcinogenesis paradigm “Epistemology of the origin of cancer”
The anti-hyperglycemic drug, Metformin, is effective in treating early stages of diabetes and has been associated with a 37% decrease in cancer incidence. While the precise mechanisms for the anti-cancer effects of Metformin remain to be elucidated, this review shows the multiplicity of its effects on interdicting signaling and crosstalk, anti-inflammatory effects and in restoring homeostasis, which, taken together, go beyond its well-known anti-hyperglycemic effect that serves as the basis for its use in type 2 diabetes. Metformin is much more than a one-trick pony. The recent discovery of several signaling pathways influenced by Metformin appears to have potential value in cancer therapy. Based on what we know at present, Metformin promotes beneficial effects attributed to its anti-inflammatory and anti-fibrotic effects largely demonstrated in vitro. Metformin activates or upregulates while it simultaneously inhibits or downregulates multiple signaling pathways of cell-cycle arrest and apoptosis accompanied by oxidative stress, which are in accordance with the 6-step sequence of carcinogenesis. Furthermore, in vivo studies in laboratory animals and in cancer patients are beginning to address the magnitude of the anti-cancer effects and delineate its anti-cancer effects. In this context, results from prior pancreatic and non-pancreatic cancer trials, which contained a significant proportion of the patient population treated with Metformin, will have to be reexamined in light of the observed anti-cancerous effects to gain additional insights. The detailed exploration of Metformin in the context of the “Disruption of signaling homeostasis induced crosstalk in the carcinogenesis paradigm Epistemology of the origin of cancer” can provide helpful insights into the anti-proliferative mechanisms and could play a relevant role in anti-cancer therapy in the future.
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