干细胞、Notch-1 信号传导和氧化应激:气道内癌症发展和恶化的地狱三重奏。天然化合物能发挥作用吗?

IF 3.3 3区 医学 Q2 ONCOLOGY
Giuseppina Chiappara, Serena Di Vincenzo, Caterina Cascio, Elisabetta Pace
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引用次数: 0

摘要

Notch-1 信号在各种粘膜表面(包括气道粘膜)的干细胞维持和修复机制中发挥着至关重要的作用。持续性损伤可诱导干细胞中的 Notch-1 信号异常激活,导致癌症发生和发展的风险增加。慢性炎症性呼吸系统疾病,包括慢性阻塞性肺病(COPD)与 Notch-1 信号的过度激活和肺癌风险的增加有关。香烟烟雾也会导致氧化应激增加,通过扩大炎症反应、激活Notch-1信号以及阻断抑制干细胞生长能力的调节机制,进一步促进癌症的发生和发展。本综述全面概述了干细胞中异常 Notch-1 信号激活和氧化应激增加对肺癌的影响。此外,还介绍了具有抗氧化特性的天然化合物可能发挥的作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Stem cells, Notch-1 signaling, and oxidative stress: a hellish trio in cancer development and progression within the airways. Is there a role for natural compounds?

Notch-1 signaling plays a crucial role in stem cell maintenance and in repair mechanisms in various mucosal surfaces, including airway mucosa. Persistent injury can induce an aberrant activation of Notch-1 signaling in stem cells leading to an increased risk of cancer initiation and progression. Chronic inflammatory respiratory disorders, including chronic obstructive pulmonary disease (COPD) is associated with both overactivation of Notch-1 signaling and increased lung cancer risk. Increased oxidative stress, also due to cigarette smoke, can further contribute to promote cancer initiation and progression by amplifying inflammatory responses, by activating the Notch-1 signaling, and by blocking regulatory mechanisms that inhibit the growth capacity of stem cells. This review offers a comprehensive overview of the effects of aberrant Notch-1 signaling activation in stem cells and of increased oxidative stress in lung cancer. The putative role of natural compounds with antioxidant properties is also described.

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来源期刊
Carcinogenesis
Carcinogenesis 医学-肿瘤学
CiteScore
9.20
自引率
2.10%
发文量
95
审稿时长
1 months
期刊介绍: Carcinogenesis: Integrative Cancer Research is a multi-disciplinary journal that brings together all the varied aspects of research that will ultimately lead to the prevention of cancer in man. The journal publishes papers that warrant prompt publication in the areas of Biology, Genetics and Epigenetics (including the processes of promotion, progression, signal transduction, apoptosis, genomic instability, growth factors, cell and molecular biology, mutation, DNA repair, genetics, etc.), Cancer Biomarkers and Molecular Epidemiology (including genetic predisposition to cancer, and epidemiology), Inflammation, Microenvironment and Prevention (including molecular dosimetry, chemoprevention, nutrition and cancer, etc.), and Carcinogenesis (including oncogenes and tumor suppressor genes in carcinogenesis, therapy resistance of solid tumors, cancer mouse models, apoptosis and senescence, novel therapeutic targets and cancer drugs).
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