Objective       To evaluate the effect of sunitinib on the proliferation and expression of phosphorylating-signal transducer and activator of transcription1 and 3 (STAT1

STAT3) in the head and neck cancer cell line PCI-13 in order to determine the role of STAT3 pathway in the antitumor activity of sunitinib.       Methods       PCI-13 cells were treated with different concentrations of sunitinib (1.25

2.5

5

10 and 20 μmol/L) for 24

48 and 72 h. Then MTT assay

i

nversion phase contrast microscopy

Wright-Giemsa staining and flow cytometry were used to calculate the growth inhibitory rate and to observe the apoptosis of PCI-13 cells. PCI-13 cells were respectively treated with 0

1

2 and 4 μmol/L sunitinib for 2

8

16 and 24 h after 48 hours’ sera starving. Then phosphorylated-STAT1 and 3 were detected with flow cytometry.       Results       Sunitinib significantly inhibited the growth of PCI-13 cells in a time- and dose-dependent manner （

P

0.05）and the highest inhibitory rate was 92%. Meanwhile

sunitinib also significantly induced apoptosis in PCI-13 cells

and the apoptotic rate was increased in a time- and dose-dependent manner（

P

0.05）. Sunitinib had no effect on the  expression of p-STAT1（

P

0.05）

but significantly suppressed the expression of p-STAT3 in a dose-dependent manner（

P

0.05）.       Conclusion       Sunitib not only inhibits the proliferation and induces the apoptosis of PCI-13 cells in a time- and dose-dependent manner

but also inhibits the phosphorylation and actitvity of STAT3

suggesting that sunitinib might induce apoptosis in PCI-13 cells by STAT/JAK pathway.