Airborne particulate matter (PM <subscript>10</subscript> ) induces cell invasion through Aryl Hydrocarbon Receptor and Activator Protein 1 (AP-1) pathway deregulation in A549 lung epithelial cells. - OpacWWW

Szczegóły
Abstrakt

Tytuł:: Airborne particulate matter (PM 10 ) induces cell invasion through Aryl Hydrocarbon Receptor and Activator Protein 1 (AP-1) pathway deregulation in A549 lung epithelial cells.
Autorzy:: Morales-Bárcenas R; Subdirección de Investigación Básica, Instituto Nacional de Cancerología, San Fernando No. 22, Tlalpan, 14080, México, D.F, México.
Sánchez-Pérez Y; Subdirección de Investigación Básica, Instituto Nacional de Cancerología, San Fernando No. 22, Tlalpan, 14080, México, D.F, México.
Santibáñez-Andrade M; Subdirección de Investigación Básica, Instituto Nacional de Cancerología, San Fernando No. 22, Tlalpan, 14080, México, D.F, México.
Chirino YI; Unidad de Biomedicina, Facultad de Estudios Superiores Iztacala, Universidad Nacional Autónoma de México, Los Reyes Iztacala, CP 54090, Tlalnepantla de Baz, Estado de México, México.
Soto-Reyes E; Departamento de Ciencias Naturales, Universidad Autónoma Metropolitana-Cuajimalpa (UAM-C), Ciudad de México, México.
García-Cuellar CM; Subdirección de Investigación Básica, Instituto Nacional de Cancerología, San Fernando No. 22, Tlalpan, 14080, México, D.F, México. .
Źródło:: Molecular biology reports [Mol Biol Rep] 2023 Jan; Vol. 50 (1), pp. 107-119. Date of Electronic Publication: 2022 Oct 29.
Typ publikacji:: Journal Article
Język:: English
Imprint Name(s):: Original Publication: Dordrecht, Boston, Reidel.
MeSH Terms:: Transcription Factor AP-1*/genetics
Particulate Matter*/toxicity
Humans ; A549 Cells ; Receptors, Aryl Hydrocarbon/genetics ; Receptors, Aryl Hydrocarbon/metabolism ; Matrix Metalloproteinase 9/genetics ; Matrix Metalloproteinase 9/metabolism ; Lung/metabolism ; Epithelial Cells/metabolism
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Contributed Indexing:: Keywords: Activator protein 1 (AP-1); Aryl hydrocarbon receptor (AhR); Cellular invasion.; MMP-9; PM10
Substance Nomenclature:: 0 (Transcription Factor AP-1)
0 (Particulate Matter)
0 (Receptors, Aryl Hydrocarbon)
EC 3.4.24.35 (Matrix Metalloproteinase 9)
Entry Date(s):: Date Created: 20221030 Date Completed: 20230131 Latest Revision: 20230202
Update Code:: 20240105
DOI:: 10.1007/s11033-022-07986-x
PMID:: 36309615
: Czasopismo naukowe

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Background: Particulate matter with an aerodynamic size ≤ 10 μm (PM 10 ) is a risk factor for lung cancer development, mainly because some components are highly toxic. Polycyclic aromatic hydrocarbons (PAHs) are present in PM 10 , such as benzo[a]pyrene (BaP), which is a well-known genotoxic and carcinogenic compound to humans, capable of activating AP-1 transcription factor family genes through the Aryl Hydrocarbon Receptor (AhR). Because effects of BaP include metalloprotease 9 (MMP-9) activation, cell invasion, and other pathways related to carcinogenesis, we aimed to demonstrate that PM 10 (10 µg/cm 2 ) exposure induces the activation of AP-1 family members as well as cell invasion in lung epithelial cells, through AhR pathway.
Methods and Results: The role of the AhR gene in cells exposed to PM 10 (10 µg/cm 2 ) and BaP (1µM) for 48 h was evaluated using AhR-targeted interference siRNA. Then, the AP-1 family members (c-Jun, Jun B, Jun D, Fos B, C-Fos, and Fra-1), the levels/activity of MMP-9, and cell invasion were analyzed. We found that PM 10 increased AhR levels and promoted its nuclear localization in A549 treated cells. Also, PM 10 and BaP deregulated the activity of AP-1 family members. Moreover, PM 10 upregulated the secretion and activity of MMP-9 through AhR, while BaP had no effect. Finally, we found that cell invasion in A549 cells exposed to PM 10 and BaP is modulated by AhR.
Conclusion: Our results demonstrated that PM 10 exposure induces upregulation of the c-Jun, Jun B, and Fra-1 activity, the expression/activity of MMP-9, and the cell invasion in lung epithelial cells, effects mediated through the AhR. Also, the Fos B and C-Fos activity were downregulated. In addition, the effects induced by PM 10 exposure were like those induced by BaP, which highlights the potentially toxic effects of the PM 10 mixture in lung epithelial cells.
(© 2022. The Author(s), under exclusive licence to Springer Nature B.V.)

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Airborne particulate matter (PM 10 ) induces cell invasion through Aryl Hydrocarbon Receptor and Activator Protein 1 (AP-1) pathway deregulation in A549 lung epithelial cells.