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
  • 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.