NDLI: Cyclophilin A inhibits A549 cell oxidative stress and apoptosis by modulating the PI3K/Akt/mTOR signaling pathway.

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Cyclophilin A inhibits A549 cell oxidative stress and apoptosis by modulating the PI3K/Akt/mTOR signaling pathway.

Content Provider	Europe PMC
Author	Ma, Zhenling Zhang, Wenwen Wu, Yaru Zhang, Menghao Wang, Lei Wang, Yihan Wang, Yi Liu, Wei
Copyright Year	2021
Abstract	AbstractThe excessive and inappropriate production of reactive oxygen species (ROS) can cause oxidative stress and is implicated in the pathogenesis of lung cancer. Cyclophilin A (CypA), a member of the immunophilin family, is secreted in response to ROS. To determine the role of CypA in oxidative stress injury, we investigated the role that CypA plays in human lung carcinoma (A549) cells. Here, we showed the protective effect of human recombinant CypA (hCypA) on hydrogen peroxide (H2O2)-induced oxidative damage in A549 cells, which play crucial roles in lung cancer. Our results demonstrated that hCypA substantially promoted cell viability, superoxide dismutase (SOD), glutathione (GSH), and GSH peroxidase (GSH-Px) activities, and attenuated ROS and malondialdehyde (MDA) production in H2O2-induced A549 cells. Compared with H2O2-induced A549 cells, Caspase-3 activity in hCypA-treated cells was significantly reduced. Using Western blotting, we showed that hCypA facilitated Bcl-2 expression and inhibited Bax, Caspase-3, Caspase-7, and PARP-1 expression. Furthermore, hCypA activates the PI3K/Akt/mTOR pathway in A549 cells in response to H2O2 stimulation. Additionally, peptidyl-prolyl isomerase activity was required for PI3K/Akt activation by CypA. The present study showed that CypA protected A549 cells from H2O2-induced oxidative injury and apoptosis by activating the PI3K/Akt/mTOR pathway. Thus, CypA might be a potential target for lung cancer therapy.
Page Count	13
ISSN	01448463
Volume Number	41
PubMed Central reference number	PMC7846964
Issue Number	1
PubMed reference number	33393627
Journal	Bioscience Reports [Biosci. Rep]
e-ISSN	15734935
DOI	10.1042/BSR20203219
Language	English
Publisher	Portland Press Ltd.
Publisher Date	2021-01-01
Access Restriction	Open
Rights License	This is an open access article published by Portland Press Limited on behalf of the Biochemical Society and distributed under the Creative Commons Attribution License 4.0 (CC BY). © 2021 The Author(s).
Subject Keyword	apoptosis Cyclophilin A oxidative stress reactive oxygen species
Content Type	Text
Resource Type	Article
Subject	Cell Biology Molecular Biology Biochemistry Biophysics

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