Objective To detect the expressions of chemokine CXCL5 and its receptor CXCR2 in hepatocellular carcinoma (HCC), investigate their relationships between CXCL5, CXCR2 and clinicopathologic features and probe into the significance in the evaluation of prognosis. Methods Immunohistochemical Envision method was utilized to detect the expressions of CXCL5 and CXCR2 in HCC , to explore their relationship between CXCL5, CXCR2 and clinicopathologic features and MVD in HCC. Results (1) The high expression rates of CXCL5 and CXCR2 protein was 64.7% and 68.6%, respectively, significantly higher than those in adjacent tissues of HCC(17.6%, 15.7%, P < 0.05). The overexpression of CXCL5 protein had correlation with tumor size, differentiation, TNM stage and vascular invasion (P < 0.05) and the overexpression of CXCR2 protein did with tumor grade and vascular invasion (P < 0.05). (2) The value of MVD was higher in HCC than that in the adjacent tissues of HCC (P < 0.05), and had positive correlation with the expressions of CXCL5, and CXCR2 proteins. (3) The higher rates of recurrence and metastasis were in the groups of higher expression of CXCL5 and CXCR2 proteins (P < 0.05). Conclusions The overexpressions of CXCL5 and CXCR2 may promote the occurrence and development of HCC as well as the neovasculation in HCC. Therefore, they can be used as markers to evaluate the prognosis of HCC.

Objective To study the role of capsaicin on improving the sensitivity of cholangiocarcinoma (CCA) cells to 5 fluorouracil(5-FU)and to investigate its molecular mechanism.Methods The MTT and animal experiment were performed to study the effect of capsaicin on the sensitivity of CCA cells to 5-FU,and the q-PCR and Western blot were performed to study its molecular mechanism.Results The effect of 5-FU inhibiting the growth of CCA cells and in vivo was significantly enhanced by capsaicin (60 μmol/L),as well as the apoptosis induced by 5-FU (P ＜ 0.01).In molecular mechanism study,capsaicin down-regulated the expression of beclinl and atg5,but inhibited the 5-FU-induced autophagy of CCA cells.In addition,capsaicin effectively increased the phosphorylation levels of S6 (S235/236) and AKT (S473).Conclusions Capsaicin can promote cell apopto sis and inhibit cell autophagy to improve the sensitivity of CCA cells to 5-FU significantly,which maybe associated with the activation of PI3K/AKT/mTOR pathway in CCA cells.