Objective      To determine the effect of CoCl

2

induced hypoxia on the epithelial-mesenchymal transition in human papillary thyroid carcinoma and investigate the role of HIF-1α in this process.       Methods      Cell vitality was evaluated by MTT assay in human papillary thyroid carcinoma NPA cells after the treatment of 50

100

150

200 and 250 μm

ol/L CoCl

2

. Morphological changes of NPA cells were observed by inverted microscopy after 150 μmol/L CoCl

2

treatment for 0

12

24 and 48 h. The expression levels of HIF-1α

E-cadherin and Vimentin were analyzed by Western blotting in NPA cells after 150 μmol/L CoCl

2

treatment for 0

3

6

12

and 24 h. The invasion and metastasis potential in NPA cells after 150 μmol/L CoCl

2

treatment for 0 and 6 h was detected by Transwell assay. Immunofluorescence was used to detect the location of HIF-1α in NPA cells.       Results      CoCl

2

treatment resulted in suppression of NPA cell vitality in a dose-dependent manner. The longer CoCl

2

was treated

NPA cells gradually acquired the morphological characteristics of mesenchymal cells. The expression of HIF-1α

E-cadherin and Vimentin was gradually enhanced in 0 to 6 h after treatment

and then declined

especially in E-cadherin. Significant differences were found in the expression levels of these proteins at 0 h and 6 h (P0.01). There were more cells that penetrated through the Transwell membrane in hypoxia group than in normoxic group (P0.01). HIF-1α translocated to the nucleus in hypoxia group

while it didn’t occur in normoxia group.       Conclusion      CoCl

2

treatment

which mimics chemical hypoxia improves the epithelial-mesenchymal transition

invasion and migration of NPA cells

which might be due to that HIF-1α mediated signal pathway regulates E-cadherin and Vimentin.