| PURPOSE : Reactive oxygen species (ROS) and the epithelial to mesenchymal transition (EMT) are key effectors in cancer metastasis.Overexpression of growth differentiation factor 11 (GDF11) is correlated with lymph node metastasis in colon cancer, but its function in cancer progression is poorly understood. In the current study, we investigated GDF11 and ROS expression in metastatic oral cancer and explored their roles in inducing EMT.METHODS: 1 ? Twenty oral squamous cell carcinoma (OSCC) patients were enrolled in a small-scale prospective study. The primary tumor tissues were collected from these patients. And the expression of GDF11 and the oxidative stress marker 8-OHdG proteins were evaluated through Immunohistochemistry method, the GDF11mRNA were evaluated through qRT-PCR and ROS production was measured by DCFH-DA fluorescent assay,the gene expression levels of EMT-related markers were determined to RT-PCR.2?SCC-9 cells, a human tongue carcinoma cell line, were treated with recombinant GDF11. Induction of EMT, expression of EMT-related markers,and the effect of ROS on EMT in SCC-9 cells were analyzed.RESULTS: 1? Overexpression of GDF11 and ROS was observed in patients with metastatic oral cancer. Downregulated expression of E-cadherin and upregulated expression of vimentin, ?-EF1, SIP-1, MMP-2, and MMP-9 were observed in patients with metastatic oral cancer, relative to their expression in patients with non-metastatic oral cancer.2.With recombinant GDF11 treatment, obvious spindle-shaped cells appeared and gene expressions of EMT-related markers were altered in SCC-9 cells. Treatment with the powerful antioxidant N-acetylcysteine (NAC) inhibited GDF11-induced EMT and cell migration.CONCLUSION: GDF11 induces EMT and cell migration with ROS involvement in SCC-9 cells. Overexpression of GDF11 and ROS is associated with metastatic oral cancer. GDF11 and ROS may participate in metastasis of oral cancer through EMT. |
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