Objective:To investigate the regulation of p53 expression by IL-17-janus protein tyrosine kinase 2/signal transducers and activators 3 of transcription（IL-17-JAK2/STAT3）signaling pathway and down-regulation of the apoptotic sensitivity to chemotherapy and to explore the mechanism of drug resistance in hepatocellular carcinoma（HCC）. Methods:Thirty cases of HCC（pathological diagnosis）and 30 cases of healthy physical examination in our hospital from May 2012 to January 2015 were chosen as research subjects.IL-17 level in serum was detected by ELISA. HepG2 cells were cultured and added to anti-IL-17 R

IL-17 and oxaliplatin co-culture for 24 hours

then the protein was exacted to detect the apoptosis related protein BAX and Bcl-2 and key nodes protein of JAK2/STAT3 signal pathway and the expression of p53 by Western blot. The expression of p53 was detected while JAK2/STAT3 pathway was blocked with AG490. Results:After chemotherapy

HCC patients serum IL-17 level [（143.96±33.20）pg/m L] was much higher than that before chemotherapy[（77.36±15.66）pg/m L] and that of healthy check-up group[（26.61±4.95）pg/m L]（P<0.05）. After HepG2 cells being cultured with anti-IL-17 R and oxaliplatin for 24 hours

the expression of BAX was increased while Bcl-2 was decreased

the expressions of p-jak2

p-STAT3 were significantly decreased while p53 was increased. After adding IL-17 to HepG2 cells

BAX was decreased while Bcl-2 was increased significantly

p-jak2

p-STAT3 were significantly increased while p53 was significantly reduced. After adding AG490 blocking agents

p53 expression was increased. Conclusion:IL-17 could regulate p53 expression through activated JAK2/STAT3 signaling pathway

which can reduce the chemotherapy sensitivity of HCC.