Loss of Caveolin-1 expression in tumor cells is associated with increased aggressiveness and cell invasion in oral squamous cell carcinoma
Nascimento, Rebeca Barros; Paiva, Katiúcia Batista Silva; Risteli, Maija; Silva, Luiz Henrique Santos; Rodini, Camila Oliveira; Rodrigues, Maria Fernanda Setúbal Destro; De Cicco, Rafael; Lopez, Rossana Verónica Mendoza; Salo, Tuula Anneli; Nunes, Fábio Daumas; Xavier, Flávia Caló Aquino (2023-05-26)
Nascimento, R.B., Paiva, K.B.S., Risteli, M. et al. Loss of Caveolin-1 Expression in Tumor Cells is Associated with Increased Aggressiveness and Cell Invasion in Oral Squamous Cell Carcinoma. Head and Neck Pathol 17, 618–630 (2023). https://doi.org/10.1007/s12105-023-01562-w
© The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2023. This version of the article has been accepted for publication, after peer review (when applicable) but is not the Version of Record and does not reflect post-acceptance improvements, or any corrections. The Version of Record is available online at: https://doi.org/10.1007/s12105-023-01562-w. Use of this Accepted Version is subject to the publisher’s Accepted Manuscript terms of use https://www.springernature.com/gp/open-research/policies/accepted-manuscript-terms.
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https://urn.fi/URN:NBN:fi-fe2023070582973
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Abstract
Background: Changes in Caveolin-1 (CAV-1) expression are related to tumorigenesis. The aim of this study was to evaluate the role of CAV-1 in tumor progression in oral squamous cell carcinoma (SCC) tissue samples and the effect of CAV-1 silencing on two oral tongue SCC (OTSCC) cell lines (SCC-25, from a primary tumor, and HSC-3 from lymph node metastases).
Methods: Mycroarray hybridization, mRNA expression, and immunohistochemistry were performed on OSCC tissue samples and corresponding non-tumoral margin tissues. The effects of CAV-1 silencing (siCAV-1) on cell viability, membrane fluidity, on the expression of epithelial to mesenchymal transition (EMT) markers and on cell migration and invasion capacity of OTSCC cell lines were evaluated.
Results: Microarray showed a greater CAV-1 expression (1.77-fold) in OSCC tumors than in non-tumoral tissues and 2.0-fold more in less aggressive OSCCs. However, significant differences in CAV-1 gene expression were not seen between tumors and non-tumoral margins nor CAV-1 with any clinicopathological parameters. CAV-1 protein was localized both in carcinoma and in spindle cells of the tumor microenvironment (TME), and CAV-1 positive TME cells were associated with smaller/more aggressive tumors, independent of the carcinoma cells’ expression. Silencing of CAV-1 increased cell viability only in SCC-25 cells. It also stimulated the invasion of HSC-3 cells and increased ECAD and BCAT mRNA in these cells; however, the protein levels of the EMT markers were not affected.
Conclusion: Decreased expression of CAV-1 by tumor cells in OSCC and an increase in the TME were associated with increased cell invasiveness and tumor aggressiveness.
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