Formoterol Exerts Anti-Cancer Effects Modulating Oxidative Stress and Epithelial-Mesenchymal Transition Processes in Cigarette Smoke Extract Exposed Lung Adenocarcinoma Cells
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Published:2023-11-08
Issue:22
Volume:24
Page:16088
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ISSN:1422-0067
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Container-title:International Journal of Molecular Sciences
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language:en
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Short-container-title:IJMS
Author:
Ferraro Maria1ORCID, Di Vincenzo Serena1ORCID, Lazzara Valentina2, Pinto Paola3, Patella Bernardo4, Inguanta Rosalinda4ORCID, Bruno Andreina1ORCID, Pace Elisabetta1ORCID
Affiliation:
1. Institute of Translational Pharmacology (IFT), National Research Council (CNR), 90146 Palermo, Italy 2. Dipartimento di Scienze Economiche, Aziendali e Statistiche, Università degli Studi di Palermo, 90100 Palermo, Italy 3. Dipartimento di Sanità Pubblica, Medicina Sperimentale e Forense, Università di Pavia, 27100 Pavia, Italy 4. Laboratorio di Chimica Fisica Applicata, Dipartimento di Ingegneria, Università di Palermo, 90128 Palermo, Italy
Abstract
Lung cancer frequently affects patients with Chronic Obstructive Pulmonary Disease (COPD). Cigarette smoke (CS) fosters cancer progression by increasing oxidative stress and by modulating epithelial-mesenchymal transition (EMT) processes in cancer cells. Formoterol (FO), a long-acting β2-agonist widely used for the treatment of COPD, exerts antioxidant activities. This study explored in a lung adenocarcinoma cell line (A549) whether FO counteracted the effects of cigarette smoke extract (CSE) relative to oxidative stress, inflammation, EMT processes, and cell migration and proliferation. A549 was stimulated with CSE and FO, ROS were evaluated by flow-cytometry and by nanostructured electrochemical sensor, EMT markers were evaluated by flow-cytometry and Real-Time PCR, IL-8 was evaluated by ELISA, cell migration was assessed by scratch and phalloidin test, and cell proliferation was assessed by clonogenic assay. CSE significantly increased the production of ROS, IL-8 release, cell migration and proliferation, and SNAIL1 expression but significantly decreased E-cadherin expression. FO reverted all these phenomena in CSE-stimulated A549 cells. The present study provides intriguing evidence that FO may exert anti-cancer effects by reverting oxidative stress, inflammation, and EMT markers induced by CS. These findings must be validated in future clinical studies to support FO as a valuable add-on treatment for lung cancer management.
Funder
Italian National Research Council (CNR); Project “SeNSO” Sicilian Micronano Tech Research and Innovation Center—SAMOTHRACE
Subject
Inorganic Chemistry,Organic Chemistry,Physical and Theoretical Chemistry,Computer Science Applications,Spectroscopy,Molecular Biology,General Medicine,Catalysis
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