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LncRNA MEG3 mediates nickel oxide nanoparticles-induced pulmonary fibrosis via suppressing TGF-β1 expression and epithelial-mesenchymal transition process.长链非编码 RNA MEG3 通过抑制 TGF-β1 表达和上皮-间充质转化过程介导氧化镍纳米颗粒诱导的肺纤维化。
Environ Toxicol. 2021 Jun;36(6):1099-1110. doi: 10.1002/tox.23109. Epub 2021 Feb 6.
2
The role of hypoxia in the tumor microenvironment and development of cancer stem cell: a novel approach to developing treatment.缺氧在肿瘤微环境及癌症干细胞发展中的作用:一种开发治疗方法的新途径。
Cancer Cell Int. 2021 Jan 20;21(1):62. doi: 10.1186/s12935-020-01719-5.
3
Competing Endogenous RNA Networks in the Epithelial to Mesenchymal Transition in Diffuse-Type of Gastric Cancer.弥漫型胃癌上皮-间质转化中的竞争性内源RNA网络
Cancers (Basel). 2020 Sep 24;12(10):2741. doi: 10.3390/cancers12102741.
4
miR-21 mediates nickel nanoparticle-induced pulmonary injury and fibrosis.miR-21 介导镍纳米颗粒诱导的肺损伤和纤维化。
Nanotoxicology. 2020 Nov;14(9):1175-1197. doi: 10.1080/17435390.2020.1808727. Epub 2020 Sep 14.
5
Epithelial-Mesenchymal Transition in Asthma Airway Remodeling Is Regulated by the IL-33/CD146 Axis.哮喘气道重塑中的上皮-间充质转化受 IL-33/CD146 轴调节。
Front Immunol. 2020 Jul 22;11:1598. doi: 10.3389/fimmu.2020.01598. eCollection 2020.
6
Nano nickel oxide promotes epithelial-mesenchymal transition through transforming growth factor β1/smads signaling pathway in A549 cells.纳米氧化镍通过转化生长因子 β1/smads 信号通路促进 A549 细胞上皮-间充质转化。
Environ Toxicol. 2020 Dec;35(12):1308-1317. doi: 10.1002/tox.22995. Epub 2020 Jul 18.
7
Hypoxia-Induced Epithelial-Mesenchymal Transition in Cancers: HIF-1α and Beyond.癌症中缺氧诱导的上皮-间质转化:HIF-1α及其他因素
Front Oncol. 2020 Apr 8;10:486. doi: 10.3389/fonc.2020.00486. eCollection 2020.
8
Exogenous hydrogen sulfide donor NaHS alleviates nickel-induced epithelial-mesenchymal transition and the migration of A549 cells by regulating TGF-β1/Smad2/Smad3 signaling.外源性硫化氢供体 NaHS 通过调节 TGF-β1/Smad2/Smad3 信号通路缓解镍诱导的 A549 细胞上皮-间充质转化和迁移。
Ecotoxicol Environ Saf. 2020 Jun 1;195:110464. doi: 10.1016/j.ecoenv.2020.110464. Epub 2020 Mar 12.
9
Nickel-induced transcriptional changes persist  post exposure through epigenetic reprogramming.镍诱导的转录变化在暴露后通过表观遗传重编程持续存在。
Epigenetics Chromatin. 2019 Dec 19;12(1):75. doi: 10.1186/s13072-019-0324-3.
10
Sanguinarine inhibits epithelial-mesenchymal transition via targeting HIF-1α/TGF-β feed-forward loop in hepatocellular carcinoma.血根碱通过靶向肝细胞癌中的 HIF-1α/TGF-β 正反馈环抑制上皮-间充质转化。
Cell Death Dis. 2019 Dec 9;10(12):939. doi: 10.1038/s41419-019-2173-1.

上皮-间充质转化:镍诱导肺部疾病的研究进展。

Epithelial-mesenchymal transition: Insights into nickel-induced lung diseases.

机构信息

Department of Environmental Medicine, New York University School of Medicine, New York, NY, 10010, USA.

Department of Environmental Medicine, New York University School of Medicine, New York, NY, 10010, USA.

出版信息

Semin Cancer Biol. 2021 Nov;76:99-109. doi: 10.1016/j.semcancer.2021.05.020. Epub 2021 May 29.

DOI:10.1016/j.semcancer.2021.05.020
PMID:34058338
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8627926/
Abstract

Nickel compounds are environmental toxicants, prevalent in the atmosphere due to their widespread use in several industrial processes, extensive consumption of nickel containing products, as well as burning of fossil fuels. Exposure to nickel is associated with a multitude of chronic inflammatory lung diseases including asthma, chronic obstructive pulmonary disease (COPD) and pulmonary fibrosis. In addition, nickel exposure is implicated in the development of nasal and lung cancers. Interestingly, a common pathogenic mechanism underlying the development of diseases associated with nickel exposure is epithelial-mesenchymal transition (EMT). EMT is a process by which the epithelial cells lose their junctions and polarity and acquire mesenchymal traits, including increased ability to migrate and invade. EMT is a normal and essential physiological process involved in differentiation, development and wound healing. However, EMT also contributes to a number of pathological conditions, including fibrosis, cancer and metastasis. Growing evidence suggest that EMT induction could be an important outcome of nickel exposure. In this review, we discuss the role of EMT in nickel-induced lung diseases and the mechanisms associated with EMT induction by nickel exposure.

摘要

镍化合物是环境毒物,由于其在许多工业过程中的广泛应用、镍制品的大量消费以及化石燃料的燃烧,它们在大气中普遍存在。接触镍与多种慢性炎症性肺部疾病有关,包括哮喘、慢性阻塞性肺疾病(COPD)和肺纤维化。此外,镍暴露还与鼻癌和肺癌的发生有关。有趣的是,镍暴露相关疾病发展的一个常见致病机制是上皮-间充质转化(EMT)。EMT 是上皮细胞失去连接和极性并获得间充质特征的过程,包括增加迁移和侵袭的能力。EMT 是一种正常且必不可少的生理过程,涉及分化、发育和伤口愈合。然而,EMT 也导致许多病理状况,包括纤维化、癌症和转移。越来越多的证据表明,EMT 的诱导可能是镍暴露的一个重要后果。在这篇综述中,我们讨论了 EMT 在镍诱导的肺部疾病中的作用,以及镍暴露诱导 EMT 的相关机制。