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Silencing of FOXA2 decreases E‐cadherin expression and is associated with lymph node metastasis in oral cancer
Author(s) -
Bow YungDing,
Wang YenYun,
Chen YukKwan,
Su ChangWei,
Hsu ChingWei,
Xiao LingYi,
Yuan ShyngShiou,
Li RueiNian
Publication year - 2020
Publication title -
oral diseases
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.953
H-Index - 87
eISSN - 1601-0825
pISSN - 1354-523X
DOI - 10.1111/odi.13282
Subject(s) - foxa2 , cdh1 , gene silencing , cadherin , cancer research , cancer , dna methylation , metastasis , medicine , immunohistochemistry , methylation , oncology , cell , pathology , gene expression , biology , gene , biochemistry , genetics
Objectives FOXA2 gene methylation links to the progression of cancers, but has not been documented in oral cancer. Herein, we explore the role of FOXA2 in the migration of oral cancer cells. Material and Methods Methylation‐specific PCR was applied for gene methylation. Wound healing and transwell experiments were tested for cell migration. FOXA2 expression in oral cancer tissues was addressed by immunohistochemistry, followed by statistical analysis of its association with clinical manifestations and patient survival. Results FOXA2 bound to the promoter of CDH1 and enhanced the expression of its gene product E‐cadherin, and decreased the cancer cell migration activity. High FOXA2 expression in oral cancer tissues was associated with high E‐cadherin expression, decreased lymph node metastasis, and increased patient survival. Conclusion FOXA2‐E‐cadherin link is involved in regulation of oral cancer cell metastasis and provides a new insight for the tumor suppressor activity of FOXA2 in oral cancer.