1. Academic Validation
  2. β-Arrestin-1 expression and epithelial-to-mesenchymal transition in laryngeal carcinoma

β-Arrestin-1 expression and epithelial-to-mesenchymal transition in laryngeal carcinoma

  • Int J Biol Markers. 2019 Mar;34(1):33-40. doi: 10.1177/1724600818813621.
Gino Marioni 1 Lorenzo Nicolè 2 Rocco Cappellesso 2 Rosario Marchese-Ragona 1 Elena Fasanaro 3 Roberto Di Carlo 1 Fabio Biagio La Torre 4 Ennio Nardello 1 Tiziana Sanavia 5 Giancarlo Ottaviano 1 Ambrogio Fassina 2
Affiliations

Affiliations

  • 1 1 Department of Neuroscience DNS, Otolaryngology Section, Padova University, Padova, Italy.
  • 2 2 Department of Medicine DIMED, University of Padova, Italy.
  • 3 3 Radiotherapy Unit, Istituto Oncologico Veneto, IOV-IRCSS, Padova, Italy.
  • 4 4 Otolaryngology Unit, Azienda Ospedaliera "S. Maria degli Angeli," Pordenone, Italy.
  • 5 5 Department of Biomedical Informatics, Harvard Medical School, Boston, MA, USA.
Abstract

Aim: The novel primary end-point of the present study was to ascertain β-arrestin-1 expression in a cohort of consecutive patients with laryngeal squamous cell carcinoma (LSCC) with information available on their cigarette-smoking habits. A secondary end-point was to conduct a preliminary clinical and pathological investigation into the possible role of β-arrestin-1 in the epithelial-to-mesenchymal transition (EMT), identified by testing for E-cadherin, Zeb1, and Zeb2 expression, in the setting of LSCC.

Methods: The expression of β-arrestin-1, E-cadherin, zeb1, and zeb2 was ascertained in 20 consecutive LSCCs.

Results: Statistical analysis showed no significant associations between β-arrestin-1 and EMT (based on the expression of E-cadherin, Zeb1, and Zeb2). The combined effect of nicotine and β-arrestin-1 was significantly associated with a shorter disease-free survival ( P=0.01) in our series of LSCC. This latter result was also confirmed in an independent, publicly available LSCC cohort ( P=0.047).

Conclusions: Further investigations on larger series (ideally in prospective settings) are needed before we can consider closer follow-up protocols and/or more aggressive treatments for patients with LSCC and a combination of nicotine exposure and β-arrestin-1 positivity in tumor cells at the time of their diagnosis. Further studies on how β-arrestin functions in Cancer via different signaling pathways might reveal potential targets for the treatment of even advanced laryngeal malignancies.

Keywords

Laryngeal carcinoma; epithelial-to-mesenchymal transition; nicotine; prognosis; β-arrestin-1.

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