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Chemokine ( CC  motif) ligand 18 ( CCL 18) is involved in remodeling of the tumor microenvironment and plays critical roles in oncogenesis, invasiveness, and metastasis. We previously investigated the overexpression of  CCL 18 in primary oral squamous cell carcinoma ( OSCC ) tissues and its association with advanced clinical stage in  OSCC  patients. However, the underlying mechanisms of this  CCL 18‐derived activity remains unidentified. This study showed exogenous  CCL 18 increased cell migration and invasion and induced cell epithelial–mesenchymal transition ( EMT ), and that E‐cadherin, an epithelial marker, decreased and N‐cadherin, a mesenchymal marker, increased, compared to negative control in  OSCC  cells. Furthermore, we detected that  CCL 18 induced the acquisition of cancer stem(‐like) cell characteristics in oral cancer cells, but also found a significantly positive correlation between the expression of  CCL 18 and Bmi‐1 ( P  < 0.001) in  OSCC  surgical specimens by immunohistochemistry analysis. The expression of octamer‐binding transcription factor 4 and Bmi‐1 were significantly upregulated, and proportions of aldehyde dehydrogenase high+  cells and  CD 133 +  cells were markedly increased in  CCL 18‐treated cells compared to untreated cells. Sphere formation ability was observably enhanced when cells were continually exposed to high levels of  CCL 18. Moreover,  CCL 18 upregulated Slug expression by stimulating the mammalian target of rapamycin ( mTOR ) signaling pathway in  OSCC  cell lines. Inhibition of the  mTOR  pathway by  INK 128, or Slug knockdown by  RNA  interference, reversed  CCL 18‐induced  EMT  and the stemness response at both molecular and functional levels. In conclusion, our data suggested that  CCL 18 upregulated Slug expression to promote  EMT  and stem cell‐like features by activating the  mTOR  pathway in oral cancer. These findings provide new potential targets for the early diagnosis and treatment of OSCC.

cancer science

Chemokine ( CC  motif) ligand 18 upregulates Slug expression to promote stem‐cell like features by activating the mammalian target of rapamycin pathway in oral squamous cell carcinoma