title: Decreased expression of ARID1A contributes to infiltrative growth of esophageal squamous cell carcinoma.
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.
authors.affiliation: Division of Advanced Surgical Science and Technology, Tohoku University Graduate School of Medicine; Department of Pathology, Tohoku University Graduate School of Medicine, Sendai, Miyagi, Japan.
authors.forename: Yohei
authors.initials: Y
authors.lastname: Ozawa
authors.forename: Yasuhiro
authors.initials: Y
authors.lastname: Nakamura
authors.forename: Fumiyoshi
authors.initials: F
authors.lastname: Fujishima
authors.forename: Saulo J A
authors.initials: SJ
authors.lastname: Felizola
authors.forename: Kenichiro
authors.initials: K
authors.lastname: Takeda
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Okamoto
authors.forename: Ken
authors.initials: K
authors.lastname: Ito
authors.forename: Hirotaka
authors.initials: H
authors.lastname: Ishida
authors.forename: Takuro
authors.initials: T
authors.lastname: Konno
authors.forename: Takashi
authors.initials: T
authors.lastname: Kamei
authors.forename: Noriaki
authors.initials: N
authors.lastname: Ohuchi
authors.forename: Hironobu
authors.initials: H
authors.lastname: Sasano
mesh_terms: D000368:Aged; D015820:Cadherins / Q000096:biosynthesis / Q000235:genetics; D002294:Carcinoma, Squamous Cell / Q000235:genetics / Q000378:metabolism* / Q000473:pathology; D004268:DNA-Binding Proteins; D058750:Epithelial-Mesenchymal Transition / Q000235:genetics; D004938:Esophageal Neoplasms / Q000235:genetics / Q000378:metabolism* / Q000473:pathology; D000077277:Esophageal Squamous Cell Carcinoma; D005260:Female; D006801:Humans; D007150:Immunohistochemistry; D053208:Kaplan-Meier Estimate; D008297:Male; D008875:Middle Aged; D009687:Nuclear Proteins / Q000096:biosynthesis*; D013534:Survival; D014157:Transcription Factors / Q000096:biosynthesis*
chemical_list: C112476:ARID1A protein, human; D015820:Cadherins; D004268:DNA-Binding Proteins; D009687:Nuclear Proteins; D014157:Transcription Factors