波形蛋白
上皮-间质转换
成釉细胞瘤
连环素
化学
癌症研究
基因敲除
病理
分子生物学
生物
细胞培养
免疫组织化学
下调和上调
医学
Wnt信号通路
信号转导
解剖
上颌骨
基因
生物化学
遗传学
作者
Jie Zhang,Yanhui Wang,Cunhui Fan,Ximei Xiao,Qian Zhang,Tao Xu,Chunmiao Jiang
出处
期刊:Oral Diseases
[Wiley]
日期:2019-08-09
卷期号:25 (8): 1964-1971
被引量:19
摘要
Abstract Objective Epithelial–mesenchymal transition (EMT) is important in the tooth development and tumor invasion. We investigated the effect of interleukin‐8 (IL‐8) on the EMT process in primary‐cultured ameloblastoma tumor cells (AM‐P) and ameloblastoma immortalized tumor cells (AM‐L) and its underlying mechanism. Methods IL‐8 levels in ameloblastomas were detected by immunofluorescence staining and ELISA. AM‐P cells and AM‐L cells were stimulated with IL‐8, and EMT transcription factors, total β‐catenin and phosphorylated‐β‐catenin (p‐β‐catenin) levels were determined by Western blot analysis and immunofluorescence staining. β‐catenin siRNA was used to knockdown β‐catenin expression in AM‐P cells and AM‐L cells stimulated with IL‐8. Results IL‐8 was highly expressed in the solid ameloblastomas. IL‐8 promoted the EMT process in ameloblastoma tumor cells in vitro, as evidenced by decreased E‐cadherin and increased vimentin, twist and zeb1 levels. IL‐8 also increased total β‐catenin and p‐β‐catenin expression in ameloblastoma tumor cells, and β‐catenin knockdown partially inhibited the EMT process in tumor cells, as evidenced by increased E‐cadherin, and decreased vimentin and zeb1 levels. Conclusions IL‐8 could promote EMT in ameloblastoma tumor cells by activating β‐catenin and its downstream transcription factor zeb1.
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