Blockade of RAGE–amphoterin signalling suppresses tumour growth and metastases

Akihiko Taguchi, David C. Blood, Gustavo del Toro, Anthony Canet, Daniel C. Lee, Wu Qu, Nozomu Tanji, Yan Lu, Evanthia Lalla, Caifeng Fu, Marion A. Hofmann, Thomas Kislinger, Mark Ingram, Amy Lu, Hidekazu Tanaka, Osamu Hori, Satoshi Ogawa, David M. Stern and Ann Marie Schmidt ()
Additional contact information
Akihiko Taguchi: College of Physicians & Surgeons, Columbia University
David C. Blood: College of Physicians & Surgeons, Columbia University
Gustavo del Toro: College of Physicians & Surgeons, Columbia University
Anthony Canet: College of Physicians & Surgeons, Columbia University
Daniel C. Lee: College of Physicians & Surgeons, Columbia University
Wu Qu: College of Physicians & Surgeons, Columbia University
Nozomu Tanji: College of Physicians & Surgeons, Columbia University
Yan Lu: College of Physicians & Surgeons, Columbia University
Evanthia Lalla: College of Physicians & Surgeons, Columbia University
Caifeng Fu: College of Physicians & Surgeons, Columbia University
Marion A. Hofmann: College of Physicians & Surgeons, Columbia University
Thomas Kislinger: College of Physicians & Surgeons, Columbia University
Mark Ingram: College of Physicians & Surgeons, Columbia University
Amy Lu: College of Physicians & Surgeons, Columbia University
Hidekazu Tanaka: Osaka University School of Medicine
Osamu Hori: Kanazawa University School of Medicine
Satoshi Ogawa: Kanazawa University School of Medicine
David M. Stern: College of Physicians & Surgeons, Columbia University
Ann Marie Schmidt: College of Physicians & Surgeons, Columbia University

Nature, 2000, vol. 405, issue 6784, 354-360

Abstract: Abstract The receptor for advanced glycation end products (RAGE), a multi-ligand member of the immunoglobulin superfamily of cell surface molecules1,2, interacts with distinct molecules implicated in homeostasis, development and inflammation, and certain diseases such as diabetes and Alzheimer's disease 3–8. Engagement of RAGE by a ligand triggers activation of key cell signalling pathways, such as p21ras, MAP kinases, NF-κB and cdc42/rac, thereby reprogramming cellular properties9,10,11. RAGE is a central cell surface receptor for amphoterin, a polypeptide linked to outgrowth of cultured cortical neurons derived from developing brain3,12,13,14,15. Indeed, the co-localization of RAGE and amphoterin at the leading edge of advancing neurites indicated their potential contribution to cellular migration, and in pathologies such as tumour invasion. Here we demonstrate that blockade of RAGE–amphoterin decreased growth and metastases of both implanted tumours and tumours developing spontaneously in susceptible mice. Inhibition of the RAGE–amphoterin interaction suppressed activation of p44/p42, p38 and SAP/JNK MAP kinases; molecular effector mechanisms importantly linked to tumour proliferation, invasion and expression of matrix metalloproteinases16,17,18,19,20,21,22,23.

Date: 2000
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DOI: 10.1038/35012626

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