口腔粘膜下纤维性变
癌症研究
DNA甲基化
医学
Wnt信号通路
甲基化
纤维化
病理
癌症
恶性转化
生物
基因表达
内科学
基因
生物化学
作者
Xiufang He,Chunjiao Xu,Xiaoshan Wu,Miaomiao Wang,Yiting Guo,Wenrui Zhang,Yumei Sun,Alisha Stha
摘要
Abstract Background Dickkopf‐1 is an inhibitor of the Wnt/β‐catenin pathway, but the role of Dickkopf‐1 in oral submucous fibrosis remains unclear. We evaluated the protein expression and gene methylation levels of dickkopf‐1 to determine the mechanism underlying abnormal Wnt/β‐catenin pathway activation. Methods Healthy mucosa, oral submucous fibrosis, oral squamous cell carcinoma, and cancer‐adjacent tissues were collected. The expression and promoter methylation levels of dickkopf‐1 were analyzed. Results The expression levels of dickkopf‐1 in oral submucous fibrosis and oral squamous cell carcinoma tissues were lower than those in healthy and cancer‐adjacent tissues. The methylation levels of the dickkopf‐1 gene in oral submucous fibrosis and oral squamous cell carcinoma tissues were higher than those in healthy and cancer‐adjacent tissues. Dickkopf‐1 expression was negatively correlated with dickkopf‐1 gene methylation. Conclusions High dickkopf‐1 methylation levels in oral submucous fibrosis and oral squamous cell carcinoma tissues may decrease dickkopf‐1 expression, which may induce an abnormal activation of the Wnt/β‐catenin pathway and oral submucous fibrosis pathogenesis.
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