Cigarette smoke extract modulates E-Cadherin, Claudin-1 and miR-21 and promotes cancer invasiveness in human colorectal adenocarcinoma cells

Autor: Claudia D'Anna, Claudia Sangiorgi, Maria Ferraro, Elisabetta Pace, C. Di Sano, S. Di Vincenzo, Paola Dino
Rok vydání: 2019
Předmět:
Zdroj: Toxicology letters 317 (2019): 102–109. doi:10.1016/j.toxlet.2019.09.020
info:cnr-pdr/source/autori:Paola Dino ; Claudia D'Anna ; Claudia Sangiorgi ; Caterina Di Sano ; Serena Di Vincenzo ; Maria Ferraro; Elisabetta Pace/titolo:Cigarette smoke extract modulates E-Cadherin, Claudin-1 and miR-21 and promotes cancer invasiveness in human colorectal adenocarcinoma cells/doi:10.1016%2Fj.toxlet.2019.09.020/rivista:Toxicology letters/anno:2019/pagina_da:102/pagina_a:109/intervallo_pagine:102–109/volume:317
ISSN: 0378-4274
DOI: 10.1016/j.toxlet.2019.09.020
Popis: Background Cigarette smoke is considered a risk factor for lung and colorectal cancer. A convincing link between epithelial-to-mesenchymal transition (EMT) with colorectal cancer progression and therapeutic resistance has emerged. Deregulated expression of E-Cadherin and Claudin-1 and increased miR-21 expression and invasiveness represent hallmarks of EMT. The effects of cigarette smoke exposure on EMT in colorectal adenocarcinoma cells are largely unknown. Aim The aim of the study is to evaluate the effect of cigarette smoke extract (CSE) on miR-21, Claudin-1 and E-Cadherin, molecules associated to EMT in colorectal cancer cells. Methods A human colorectal adenocarcinoma cell line (Caco-2) was treated with CSE at different concentration (5% and 10%) and for different time points (3 h and 24 h). Metabolic activity (by MTS assay), cell necrosis/cell apoptosis (evaluating Propidium Iodide/Annexin V expression by flow cytometry), miR-21, Claudin-1 and E-Cadherin gene expression were evaluated by Real time PCR. Cell permeability, actin polymerization and cancer cell migration was assessed by Trans-Epitelial Electrical Resistance (TEER), Phalloidin expression and matrigel system, respectively. Results CSE at all the tested concentrations and at all time points reduced cell necrosis. CSE at 10% increased miR-21 and reduced the metabolic activity, cell necrosis, Claudin-1 and E-cadherin mRNA at 3 h. Cell permeability, actin polymerization and cancer cell migration were all increased upon CSE exposure. Conclusion These results showed that CSE increasing miR-21, Claudin-1 and E-Cadherin and enhancing the aggressiveness of cancer cells, may concur to colorectal cancer progression.
Databáze: OpenAIRE