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Blockade von CXC Chemokinen hemmt die durch Pankreaskarzinomzellen induzierte Angiogenese

Chemokine blockade inhibits pancreatic cancer cell-induced angiogenesis

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Part of the book series: Deutsche Gesellschaft für Chirurgie ((FORUMBAND,volume 33))

Abstract

Background: A central feature of all solid tumor growth is the presence of neovascularization. The CXC chemokines GRO-γ/CXCL3, ENA-78/CXCL5, and IL-8/CXCL8 have profound angiogenic potential mediated through the CXCR2 receptor. The role of these proteins in pancreatic cancer biology is unknown. Methods: The aim of the present study was to evaluate the expression of the chemokines CXCL3, CXCL5, and CXCL8 in three human pancreatic cancer (PaCa) cell lines and to determine the role of these proteins in PaCa angiogenesis. Secreted CXC protein levels in the supernatant (SN) of the cell lines were analyzed by ELISA. A rat corneal micropocket model was used to determine the angiogenic potential of these secreted CXC chemokines. Results: ELISA confirmed expression of all three tested CXC chemokines in the supernatant of two cell lines. In the corneal micropocket assay, neovascularization was induced using pelleted SN of all three cell lines. Using an anti-CXCR2 antibody, neovascularization was significantly inhibited in the high expressing BxPC-3 cell line samples. Conclusions: Human PaCa cell lines secrete the angiogenic CXC chemokines CXCL3, CXCL5, and CXCL8. The dominant angiogenic protein, however, varies between cell lines and likely includes proteins outside the CXC family.

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Correspondence to M. N. Wente .

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© 2004 Springer-Verlag Berlin Heidelberg

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Wente, M.N., Reber, H.A., Hines, O.J., Strieter, R.M., Büchler, M.W., Friess, H. (2004). Blockade von CXC Chemokinen hemmt die durch Pankreaskarzinomzellen induzierte Angiogenese. In: Ulrich, B., Jauch, KW., Bauer, H., Menger, M.D., Laschke, M., Slotta, J. (eds) Chirurgisches Forum 2004. Deutsche Gesellschaft für Chirurgie, vol 33. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-18547-2_8

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  • DOI: https://doi.org/10.1007/978-3-642-18547-2_8

  • Publisher Name: Springer, Berlin, Heidelberg

  • Print ISBN: 978-3-540-20027-7

  • Online ISBN: 978-3-642-18547-2

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