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炎症相关致癌作用的化学预防策略：现状与未来方向

Chemopreventive Strategies for Inflammation-Related Carcinogenesis: Current Status and Future Direction.

作者信息

Kanda Yusuke, Osaki Mitsuhiko, Okada Futoshi

机构信息

Division of Pathological Biochemistry, Tottori University Faculty of Medicine, Yonago, Tottori 683-8503, Japan.

Chromosome Engineering Research Center, Tottori University, Yonago, Tottori 683-8503, Japan.

出版信息

Int J Mol Sci. 2017 Apr 19;18(4):867. doi: 10.3390/ijms18040867.

DOI:10.3390/ijms18040867
PMID:28422073
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5412448/
Abstract

A sustained and chronically-inflamed environment is characterized by the presence of heterogeneous inflammatory cellular components, including neutrophils, macrophages, lymphocytes and fibroblasts. These infiltrated cells produce growth stimulating mediators (inflammatory cytokines and growth factors), chemotactic factors (chemokines) and genotoxic substances (reactive oxygen species and nitrogen oxide) and induce DNA damage and methylation. Therefore, chronic inflammation serves as an intrinsic niche for carcinogenesis and tumor progression. In this article, we summarize the up-to-date findings regarding definitive/possible causes and mechanisms of inflammation-related carcinogenesis derived from experimental and clinical studies. We also propose 10 strategies, as well as candidate agents for the prevention of inflammation-related carcinogenesis.

摘要

持续的慢性炎症环境的特征是存在异质性炎症细胞成分，包括中性粒细胞、巨噬细胞、淋巴细胞和成纤维细胞。这些浸润细胞产生生长刺激介质（炎性细胞因子和生长因子）、趋化因子（趋化因子）和遗传毒性物质（活性氧和氮氧化物），并诱导DNA损伤和甲基化。因此，慢性炎症是致癌作用和肿瘤进展的内在生态位。在本文中，我们总结了来自实验和临床研究的关于炎症相关致癌作用的确切/可能原因和机制的最新发现。我们还提出了10种预防炎症相关致癌作用的策略以及候选药物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f572/5412448/51742fdf336a/ijms-18-00867-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f572/5412448/bfa9c00f7a63/ijms-18-00867-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f572/5412448/b52df8f3fd54/ijms-18-00867-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f572/5412448/6794dafcaa90/ijms-18-00867-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f572/5412448/51742fdf336a/ijms-18-00867-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f572/5412448/bfa9c00f7a63/ijms-18-00867-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f572/5412448/b52df8f3fd54/ijms-18-00867-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f572/5412448/6794dafcaa90/ijms-18-00867-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f572/5412448/51742fdf336a/ijms-18-00867-g004.jpg

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本文引用的文献

[1]
Inflammasomes in Inflammation-Induced Cancer.

Front Immunol. 2017-3-15

[2]
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J Hematol Oncol. 2017-3-9

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J Hematol Oncol. 2017-2-28

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Int Immunopharmacol. 2016-11

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