Impact Factor 3.201 | CiteScore 3.22
More on impact ›

Review ARTICLE Provisionally accepted The full-text will be published soon. Notify me

Front. Physiol. | doi: 10.3389/fphys.2019.01404

PM2.5, Fine Particulate Matter: A Novel Player in the Epithelial-Mesenchymal Transition?

Zihan Xu1 and  Xiaobei Deng1*
  • 1School of Public Health, Shanghai Jiao Tong University, China

Epithelial-mesenchymal transition (EMT) refers to the conversion of epithelial cells to mesenchymal phenotype, which endows the epithelial cells with enhanced migration, invasion and extracellular matrix production abilities. These characteristics link EMT with the pathogenesis of organ fibrosis and cancer progression. Recent studies have preliminarily established that fine particulate matter with an aerodynamic diameter less than 2.5 μm (PM2.5) is correlated with EMT initiation. In this pathological process, PM2.5 particles, excessive reactive oxygen species (ROS) derived from PM2.5 and certain components in PM2.5, such as ions and polyaromatic hydrocarbons (PAHs), have been implicated as potential EMT mediators that are linked to the activation of TGF-β/SMAD, NF-κB, GF/ERK, GF/PI3K/Akt, Wnt/β-Catenin, Notch, Hedgehog, HMGB1-RAGE and AHR signaling cascades and to cytoskeleton rearrangement. These pathways directly and indirectly transduce pro-EMT signals that regulate EMT-related gene expression in epithelial cells, finally inducing the characteristic alterations in morphology and functions of epithelia. In addition, novel associations between autophagy, ATP citrate lyase (ACLY) and exosomes with PM2.5-induced EMT has also been summarized. However, some debates and paradoxes remain to be consolidated. This review discusses the potential molecular mechanisms underlying PM2.5-induced EMT, which might account for the latent role of PM2.5 in cancer progression and fibrogenesis.

Keywords: PM2.5, EMT, Cancer, Fibrosis, signaling, Wnt / b-catenin, exosome, RTK - receptor tyrosine kinase, NFkB, ACLY ATP citrate lyase, NAC (N-acetylcysteine), Air Pollution, Molecular toxicology, TGF-β, TGF-β/Smad pathway, Cytoskeleton, Autopaghy, epigenetics, lncRNA, miRNA, DNAmethylation, Ca2+, AhR (Aryl hydrocarbon Receptor), PAH - carcinogenic, mutagenic and immunodepressive chemical

Received: 29 Apr 2019; Accepted: 31 Oct 2019.

Copyright: © 2019 Xu and Deng. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

* Correspondence: Dr. Xiaobei Deng, School of Public Health, Shanghai Jiao Tong University, Shanghai, China, dengxiaobei@sjtu.edu.cn