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Acetaldehyde Induced Cell Damage and Genotoxic Effects by Modulating PI3K/AKT and MAPK/ERK Pathways in Human Lung Epithelial Cells

ABSTRACT: Long-term acetaldehyde exposure is associated with cell death, oxidative stress, and DNA damage in lung injury such as chronic obstructive pulmonary disease and respiratory distress syndrome, but the signal transduction mechanism linking key processes remains largely unknown. This study aims to reveal molecular mechanisms of cytotoxicity and genotoxicity induced by acetaldehyde based on human bronchial epithelial cells. Firstly, RNA-seq analysis indicated that differentially expressed genes are most enriched in MAPK/ERK and PI3K/AKT pathways. Secondly, significant up-regulation of four key signaling proteins was confirmed. Subsequently, we found that inhibitors of these pathways could significantly reduce cytotoxicity, oxidative stress, and genotoxicity induced by acetaldehyde. Finally, gene silencing was employed to further validate the importance of these pathways, and toxic effects were more effectively alleviated. Our research suggests that acetaldehyde-induced cell damage and genotoxic effects through PI3K/AKT and MAPK/ERK pathways, provide new insights into toxic mechanisms of acetaldehyde-induced lung injury.

ORGANISM(S): Homo sapiens

PROVIDER: GSE289892 | GEO | 2025/02/21

REPOSITORIES: GEO

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Project description:Pappalardo2016 - PI3K/AKT and MAPK Signaling Pathways in Melanoma Cancer This model is described in the article: Computational Modeling of PI3K/AKT and MAPK Signaling Pathways in Melanoma Cancer. Pappalardo F, Russo G, Candido S, Pennisi M, Cavalieri S, Motta S, McCubrey JA, Nicoletti F, Libra M. PLoS ONE 2016; 11(3): e0152104 Abstract: Malignant melanoma is an aggressive tumor of the skin and seems to be resistant to current therapeutic approaches. Melanocytic transformation is thought to occur by sequential accumulation of genetic and molecular alterations able to activate the Ras/Raf/MEK/ERK (MAPK) and/or the PI3K/AKT (AKT) signalling pathways. Specifically, mutations of B-RAF activate MAPK pathway resulting in cell cycle progression and apoptosis prevention. According to these findings, MAPK and AKT pathways may represent promising therapeutic targets for an otherwise devastating disease.Here we show a computational model able to simulate the main biochemical and metabolic interactions in the PI3K/AKT and MAPK pathways potentially involved in melanoma development. Overall, this computational approach may accelerate the drug discovery process and encourages the identification of novel pathway activators with consequent development of novel antioncogenic compounds to overcome tumor cell resistance to conventional therapeutic agents. The source code of the various versions of the model are available as S1 Archive. This model is hosted on BioModels Database and identified by: MODEL1609190000. To cite BioModels Database, please use: BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models. To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. Please refer to CC0 Public Domain Dedication for more information.

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Acetaldehyde Induced Cell Damage and Genotoxic Effects by Modulating PI3K/AKT and MAPK/ERK Pathways in Human Lung Epithelial Cells

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