Objective      To determine the effects of interleukin-6 (IL-6) on the cell proliferation

invasion

migration and epithelial-mesenchymal transition in human esophageal carcinoma cells.       Methods      The human esophageal carcinoma Eca-109 cells were treated with IL-6 at a dose of 0

25

50 and 100 ng/mL

cell proliferation

migration and invasion were detected by MTT assay

cell scratch test and Transwell chamber assay respectively. The mRNA expression of E-cadherin

N-cadherin

Vimentin and Twist1 were evaluated by real-time quantitative PCR. The protein expression levels of Stat3

p-Stat3

E-cadherin

N-cadherin

Vimentin and Twist1 were detected by Western blotting.       Results      Compared with control group (0 ng/mL IL-6 treatment)

the cell proliferation was in a dose- and time-dependent manner when the Eca-109 cells were treated by IL-6 at 25

50 and 100 ng/mL for 1 to 5 d (P0.05

0.01). IL-6 at 0

25 and 50 ng/mL resulted in cell 24-hour migration distance of 18.20±0.89

23.77±0.40 and 25.27±0.93 mm respectively

with the 2 later doses significantly longer than the former (P0.05). IL-6 of above doses also resulted in the number of 24-hour Matrigel-permeating Eca-109 cells of 70.33±2.36

103.00±3.51 and 118.00±4.00 /HP

respectively

with the number in the 2 later groups significantly larger than in the former group (P0.05). Real time RT-PCR showed that the mRNA expression levels of N-cadherin

Vimentin and Twist1 were significantly increased and the mRNA expression level of E-cadherin was decreased in IL-6 treatment groups (25 and 50 ng/mL)

significantly different from those in 0 ng/mL group (P0.05). Western blotting showed that the protein levels of p-Stat3

N-cadherin

Vimentin and Twist1 were significantly increased

and that of E-cadherin was decreased

while that of Stat3 had no change in IL-6 treatment groups (25 and 50 ng/mL) when compared with 0 ng/mL group (P0.05).       Conclusion      IL-6 promotes the cell proliferation

invasion

migration and epithelial mesenchymal transition in human esophageal carcinoma cells by constitutively activating Stat3

up-regulating Twist1

and regulating EMT proteins (E-cadherin

N-cadherin and Vimentin).