This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Camp, E. R. Articles by Ellis, L. M. Search for Related Content PubMed PubMed Citation Articles by Camp, E. R. Articles by Ellis, L. M.

RON, a Tyrosine Kinase Receptor Involved in Tumor Progression and Metastasis

¹ Department of Surgical Oncology, The University of Texas M. D. Anderson Cancer Center, Unit 444, PO Box 301402, Houston, Texas 77230-1402
² Department of Cancer Biology, The University of Texas M. D. Anderson Cancer Center, 7777 Knight Road, Houston, Texas 77054

Correspondence: Address correspondence and reprint requests to: Lee M. Ellis, MD; E-mail: lellis{at}mdanderson.org.

ABSTRACT

Tyrosine kinase receptors mediate many critical cellular functions that contribute to tumor progression and metastasis and thus are potential targets for molecular-based cancer therapy. As has been found for many receptor tyrosine kinases, RON (recepteur d’origine nantais) and its ligand, macrophage-stimulating protein, have recently been implicated in the progression and metastasis of tumors. In in vitro experiments using colon and breast cancer cell lines, overexpression of RON led to increased invasion and migration of cancer cells and prevented apoptosis and anoikis. In addition, transgenic mice engineered to overexpress RON in the lung epithelium developed multiple pulmonary tumors, suggesting a role for RON in tumorigenesis. In human cancer specimens, increased RON expression has been demonstrated in colon, breast, ovarian, and lung tumors. Therefore, therapies designed to inhibit RON activation may hinder critical tumor survival mechanisms and play a role in the treatment of advanced disease.

Key Words: RON • Macrophage-stimulating protein • Cancer • Tyrosine kinase receptor

This article has been cited by other articles:

				M. Narasimhan and S. Ammanamanchi Curcumin Blocks RON Tyrosine Kinase-Mediated Invasion of Breast Carcinoma Cells Cancer Res., July 1, 2008; 68(13): 5185 - 5192. [Abstract] [Full Text] [PDF]

				S. Zhao, S. Ammanamanchi, M. Brattain, L. Cao, A. Thangasamy, J. Wang, and J. W. Freeman Smad4-dependent TGF-{beta} Signaling Suppresses RON Receptor Tyrosine Kinase-dependent Motility and Invasion of Pancreatic Cancer Cells J. Biol. Chem., April 25, 2008; 283(17): 11293 - 11301. [Abstract] [Full Text] [PDF]

				K. Zhang, H.-P. Yao, and M.-H. Wang Activation of RON differentially regulates claudin expression and localization: role of claudin-1 in RON-mediated epithelial cell motility Carcinogenesis, March 1, 2008; 29(3): 552 - 559. [Abstract] [Full Text] [PDF]

				A. Thangasamy, J. Rogge, and S. Ammanamanchi Regulation of RON Tyrosine Kinase-mediated Invasion of Breast Cancer Cells J. Biol. Chem., February 29, 2008; 283(9): 5335 - 5343. [Abstract] [Full Text] [PDF]

				J. M. O'Toole, K. E. Rabenau, K. Burns, D. Lu, V. Mangalampalli, P. Balderes, N. Covino, R. Bassi, M. Prewett, K. J. Gottfredsen, et al. Therapeutic Implications of a Human Neutralizing Antibody to the Macrophage-Stimulating Protein Receptor Tyrosine Kinase (RON), a c-MET Family Member. Cancer Res., September 15, 2006; 66(18): 9162 - 9170. [Abstract] [Full Text] [PDF]