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pmid28249915      Ann+Clin+Lab+Sci 2017 ; 47 (1): 40-46
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  • Cobalt Chloride-induced Hypoxia Induces Epithelial-mesenchymal Transition in Renal Carcinoma Cell Lines #MMPMID28249915
  • Zhang N; Hong B; Zhou C; Du X; Chen S; Deng X; Duoerkun S; Li Q; Yang Y; Gong K
  • Ann Clin Lab Sci 2017[Jan]; 47 (1): 40-46 PMID28249915show ga
  • 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 CoCl(2) was used to simulate hypoxia. Cells were cultured with different concentrations of CoCl(2). Morphology and changes in cytoactivity were observed. After CoCl2 treatment, the expression of HIF-1alpha and the changes of EMT-related molecules (E-cadherin, fibronectin) were detected. RESULTS: Cell conjunctions of CoCl(2)-treated groups were loose and scattered compared to the control. CoCl(2) did not promote or attenuate the viability of A498 cells at low dosage, but when the concentration of CoCl(2) reached 250 muM, cell activity gradually declined. In contrast, CoCl(2) induced 786-O cell proliferation in the range of 50 mu M-200 mu M, but inhibited cell growth at dosages higher than 200 muM. The expression of E-cadherin was significantly down-regulated, and fibronectin was up-regulated in both A498 and 786-O cell lines under CoCl(2)-simulated hypoxia in comparison with normoxic conditions (P<0.01). CONCLUSIONS: CoCl(2)-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.
  • |Carcinoma, Renal Cell/metabolism/*pathology[MESH]
  • |Cell Hypoxia/drug effects[MESH]
  • |Cell Line, Tumor[MESH]
  • |Cell Proliferation/drug effects[MESH]
  • |Cell Shape/drug effects[MESH]
  • |Cell Survival/drug effects[MESH]
  • |Cobalt/*pharmacology[MESH]
  • |Epithelial-Mesenchymal Transition/*drug effects[MESH]
  • |Humans[MESH]
  • |Hypoxia-Inducible Factor 1, alpha Subunit/metabolism[MESH]


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