Decreased Expression of ARID1A Contributes to Infiltrative Growth of Esophageal Squamous Cell Carcinoma

Access this Article

Search this Article

Author(s)

    • Ozawa Yohei
    • Division of Advanced Surgical Science and Technology, Tohoku University Graduate School of Medicine|Department of Pathology, Tohoku University Graduate School of Medicine
    • Kamei Takashi
    • Division of Advanced Surgical Science and Technology, Tohoku University Graduate School of Medicine
    • Ohuchi Noriaki
    • Division of Advanced Surgical Science and Technology, Tohoku University Graduate School of Medicine
    • Sasano Hironobu
    • Department of Pathology, Tohoku University Graduate School of Medicine|Department of Pathology, Tohoku University Hospital
    • Okamoto Hiroshi
    • Division of Advanced Surgical Science and Technology, Tohoku University Graduate School of Medicine
    • Ito Ken
    • Division of Advanced Surgical Science and Technology, Tohoku University Graduate School of Medicine|Department of Pathology, Tohoku University Hospital
    • Ishida Hirotaka
    • Division of Advanced Surgical Science and Technology, Tohoku University Graduate School of Medicine|Department of Pathology, Tohoku University Graduate School of Medicine
    • Konno Takuro
    • Division of Advanced Surgical Science and Technology, Tohoku University Graduate School of Medicine|Department of Pathology, Tohoku University Hospital

Abstract

The clinical outcome for esophageal squamous cell carcinoma (ESCC) patients is often poor because of the invasive nature of this tumor type. AT-rich interactive domain 1A (ARID1A) functions as a tumor suppressor, and its gene mutation has been reported in various human malignancies. ARID1A is a non-catalytic subunit of the SWItch/Sucrose Non Fermentable (SWI/SNF) chromatin-remodeling complex that regulates gene transcription. Decreased expression of ARID1A protein has been reported to decrease the expression of E-cadherin, an adhesion protein. However, the correlation between ARID1A and E-cadherin expression status in ESCC remains largely unknown. To address this issue, we examined the expression of ARID1A and E-cadherin in tumor specimens excised from 83 ESCC patients using immunohistochemical analysis. The intensity of the ARID1A immunoreactivity was significantly lower in tumors with a growth pattern characterized by ill-defined borders than that in tumors with an expansive growth pattern having a well-demarcated border or tumors with an intermediate growth pattern. Thus, decreased ARID1A immunoreactivity correlated with infiltrative growth of ESCC. In contrast, E-cadherin status did not correlate with the infiltrative growth pattern of ESCC. Moreover, ARID1A expression status did not significantly correlate with any of other clinicopathological factors, E-cadherin expression levels, or the clinical outcome of the patients. On the other hand, the patients with tumors expressing low levels of E-cadherin exhibited significantly lower survival rates than those with high expression. In conclusion, reduced ARID1A expression in tumor tissues contributes to infiltrative growth of ESCC, irrespective of E-cadherin expression levels.

Journal

  • The Tohoku Journal of Experimental Medicine

    The Tohoku Journal of Experimental Medicine 235(3), 185-191, 2015

    Tohoku University Medical Press

Codes

  • NII Article ID (NAID)
    130004822443
  • Text Lang
    ENG
  • ISSN
    0040-8727
  • Data Source
    J-STAGE 
Page Top