dc.contributor.author | Longhin, E. | |
dc.contributor.author | Camatini, M. | |
dc.contributor.author | Bersaas, Audun Trygge Haugen | |
dc.contributor.author | Mantecca, P. | |
dc.contributor.author | Mollerup, Steen Kristen | |
dc.date.accessioned | 2024-08-30T08:05:41Z | |
dc.date.available | 2024-08-30T08:05:41Z | |
dc.date.created | 2018-07-13T11:22:59Z | |
dc.date.issued | 2018 | |
dc.identifier.citation | Archives of Toxicology. 2018, 92 (9), 2923-2933. | |
dc.identifier.issn | 0340-5761 | |
dc.identifier.uri | https://hdl.handle.net/11250/3149246 | |
dc.description.abstract | Exposure to particulate matter (PM) has been related to the onset of adverse health effects including lung cancer, but the underlying molecular mechanisms are still under investigation. Epithelial-to-mesenchymal transition (EMT) is regarded as a crucial step in cancer progression. In a previous study, we reported EMT-related responses in the human bronchial epithelial cell line HBEC3-KT, exposed to Milan airborne winter PM2.5. We also found a strong modulation of SERPINB2, encoding for the PAI-2 protein and previously suggested to play an important role in cancer. Here we investigate the role of SERPINB2/PAI-2 in the regulation of EMT-related effects induced by PM exposure in HBEC3-KT. PM exposure (up to 10 µg/cm2) increased SERPINB2 expression, reduced cell migration and induced morphological alterations in HBEC3-KT. Changes in actin structure and cadherin-1 relocalization were observed in PM-exposed samples. Knockdown of SERPINB2 by siRNA down-regulated the CDH1 gene expression, as well as PAI-2 and cadherin-1 protein expression. SERPINB2 knockdown also increased cell migration rate, and counteracted the PM-induced reduction of cell migration and alteration of cell morphology. SERPINB2 was found to be greatly down-regulated in a HBEC2-KT transformed cell line, supporting the importance of this gene in the regulation of EMT. In conclusion, here we show that PAI-2 regulates CDH1 gene/cadherin-1 protein expression in bronchial HBEC3-KT cells, and this mechanism might be involved in the regulation of cell migration. SERPINB2 down-regulation should be considered part of EMT, and the over-expression of SERPINB2 in PM-exposed samples might be interpreted as an initial protective mechanism. | |
dc.description.abstract | The role of SerpinB2 in human bronchial epithelial cells responses to particulate matter exposure | |
dc.language.iso | eng | |
dc.title | The role of SerpinB2 in human bronchial epithelial cells responses to particulate matter exposure | |
dc.title.alternative | The role of SerpinB2 in human bronchial epithelial cells responses to particulate matter exposure | |
dc.type | Peer reviewed | |
dc.type | Journal article | |
dc.description.version | publishedVersion | |
dc.source.pagenumber | 2923-2933 | |
dc.source.volume | 92 | |
dc.source.journal | Archives of Toxicology | |
dc.source.issue | 9 | |
dc.identifier.doi | 10.1007/s00204-018-2259-z | |
dc.identifier.cristin | 1597092 | |
cristin.ispublished | true | |
cristin.fulltext | original | |
cristin.qualitycode | 1 | |