炎症小体在结直肠癌信号转导过程中受表观遗传和自噬机制的影响

G. Műzes, F. Sipos
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引用次数: 0

摘要

炎症体主要通过诱导周围肿瘤微环境中的炎症来促进结直肠癌信号转导。炎症体在炎症中的作用正受到越来越多的关注,因为炎症除了诱发组织损伤外,还具有原瘤效应。炎症小体的功能十分复杂,受多层调控。表观遗传过程会影响参与控制炎症小体或后续信号级联的基因的功能或表现。研究人员对表观遗传机制在调控中的意义进行了深入研究,因为它们包含多个潜在的治疗靶点。炎性体和自噬之间的调控相互作用错综复杂,既有有利的一面,也有有害的一面。这两个实体之间的调控也包含多个治疗靶点。炎性体的激活、自噬和表观遗传学改变之间的关系非常复杂,涉及多个相互关联的途径。本文简要概述了有关表观遗传学和自噬如何控制炎性体的最新研究,并特别关注它们在结直肠癌中的作用。根据最新发现,我们还概述了针对这一复杂网络的最新治疗思路。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Inflammasomes Are Influenced by Epigenetic and Autophagy Mechanisms in Colorectal Cancer Signaling
Inflammasomes contribute to colorectal cancer signaling by primarily inducing inflammation in the surrounding tumor microenvironment. Its role in inflammation is receiving increasing attention, as inflammation has a protumor effect in addition to inducing tissue damage. The inflammasome’s function is complex and controlled by several layers of regulation. Epigenetic processes impact the functioning or manifestation of genes that are involved in the control of inflammasomes or the subsequent signaling cascades. Researchers have intensively studied the significance of epigenetic mechanisms in regulation, as they encompass several potential therapeutic targets. The regulatory interactions between the inflammasome and autophagy are intricate, exhibiting both advantageous and harmful consequences. The regulatory aspects between the two entities also encompass several therapeutic targets. The relationship between the activation of the inflammasome, autophagy, and epigenetic alterations in CRC is complex and involves several interrelated pathways. This article provides a brief summary of the newest studies on how epigenetics and autophagy control the inflammasome, with a special focus on their role in colorectal cancer. Based on the latest findings, we also provide an overview of the latest therapeutic ideas for this complex network.
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