Objective: To establish epithelial-mesenchymal transition (EMT) models in renal cell carcinoma (RCC) cell lines.
Materials and methods: The RCC cell lines A498 and 786-O were used in the experiment and CoCl2 was used to simulate hypoxia. Cells were cultured with different concentrations of CoCl2. Morphology and changes in cytoactivity were observed. After CoCl2 treatment, the expression of HIF-1α and the changes of EMT-related molecules (E-cadherin, fibronectin) were detected.
Results: Cell conjunctions of CoCl2-treated groups were loose and scattered compared to the control. CoCl2 did not promote or attenuate the viability of A498 cells at low dosage, but when the concentration of CoCl2 reached 250 μM, cell activity gradually declined. In contrast, CoCl2 induced 786-O cell proliferation in the range of 50 μ M-200 μ M, but inhibited cell growth at dosages higher than 200 μM. The expression of E-cadherin was significantly down-regulated, and fibronectin was up-regulated in both A498 and 786-O cell lines under CoCl2-simulated hypoxia in comparison with normoxic conditions (P<0.01).
Conclusions: CoCl2-induced hypoxia could induce EMT in RCC cell lines. The models will help us further study the mechanisms of EMT and investigate novel therapeutic targets to inhibit tumor invasion and metastasis.
Keywords: E-cadherin; Epithelial-mesenchymal transition; Fibronectin; Hypoxia; Renal cell carcinoma.
© 2017 by the Association of Clinical Scientists, Inc.