Background
Gemcitabine (Gem) is currently the leading therapeutic for pancreatic cancer (PaCa) treatment, but there still is a problem of the acquisition of resistance against Gem. On the other hand, we previously reported the important role of chemokines in PaCa angiogenesis. In this study, we demonstrated the relation between chemokines and the resistance to Gem.

Material and Methods
(1) The concentration of chemokines in supernatant of PaCa was measured by ELISA. (2) The alteration of proliferation of PaCa or HUVEC by chemokine was examined by MTS-assay. (3) After the establishment of Gem resistant PaCa cell lines (PaCa-Gem-R), we compared the proliferation of PaCa-Gem-R with PaCa cell lines which were sensitive to Gem (PaCa-Gem-S). (4) The expression of chemokine in PaCa-Gem-R or PaCa-Gem-S was examined by cytokine array. (5) The angiogenic ability of PaCa-Gem-R or PaCa-Gem-S was determined by in vitro angiogenesis assay.

Result
(1) The production of chemokine in PaCa was higher compared with HPDE. (2) HUVEC proliferation was enhanced by chemokine but not PaCa proliferation. (3) There was no significant difference of proliferation between PaCa-Gem-R and PaCa-Gem-S. (4) The angiogenic ability of PaCa-Gem-R was higher than PaCa-Gem-S, and the angiogenic ability was inhibited by CXCL8 Ab.

Conclusion
The expression of chemokine was enhanced by the acquisition of Gem-resistance. The regulation of chemokine would become a potential therapeutic target in Gem resisted PaCa.