Journal
ORAL DISEASES
Volume 25, Issue 8, Pages 1964-1971Publisher
WILEY
DOI: 10.1111/odi.13173
Keywords
ameloblastoma; epithelial-mesenchymal transition; interleukin-8; zeb1; beta-catenin
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Funding
- Natural Science Foundation of Shandong Province [ZR2017BH098]
- China Postdoctoral Science Foundation [2018M642620]
- National Natural Science Foundation of China [81700992]
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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 beta-catenin and phosphorylated-beta-catenin (p-beta-catenin) levels were determined by Western blot analysis and immunofluorescence staining. beta-catenin siRNA was used to knockdown beta-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 beta-catenin and p-beta-catenin expression in ameloblastoma tumor cells, and beta-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 beta-catenin and its downstream transcription factor zeb1.
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