Department:
Department of Oncology and Diagnostic Sciences, Dental School
UMGCC Research Program:
Molecular and Structural Biology Program
Education/Training:
College Degree:
B.A., Cornell University
Medical Degree:
D.D.S., State University of New York at Stony Brook, School of Dental Medicine
Post Doctoral
Degree:
D.M.Sc., Oral Biology, Harvard University School of Dental Medicine
Residency:
Washington, D.C., V.A. Hospital
Fellowship:
American Academy of Oral and Maxillofacial Pathology
Certification:
Oral and Maxillofacial Pathology
Contact
Information:
Mailing Address:
Department of Oncology and Diagnostic Sciences
University of Maryland, Baltimore
Dental School
650 West Baltimore Street, 7-North
Baltimore, Maryland 21201
Email:
jbasile@umaryland.edu
Phone:
410-706-7628
Fax:
410-706-0519
Research Interests:
Similarities in the patterns of branching of blood vessels and nerves during growth and development have been acknowledged for some time. Biochemical and genetic confirmation of these anatomical findings has emerged more recently with the identification of certain molecules that control axonal growth in the developing nervous system as regulators of blood vessel development as well. My work focuses on Semaphorin 4D (Sema4D) and it's receptor, Plexin-B1, proteins originally shown to transmit axonal guidance cues, and their role in tumor-induced angiogenesis.
We have recently observed that Plexin-B1 is highly expressed in endothelial cells where it strongly promotes an angiogenic phenotype when bound by Sema4D. Interestingly, we have also observed that Sema4D is overexpressed by the transformed epithelial cells of many different carcinomas, including head and neck squamous cell carcinoma (HNSCC). Taken together, these findings suggest that the class IV semaphorins may play a role in tumor-induced angiogenesis. However, the factors responsible for transcriptional regulation of Sema4D and the pathways activated by Plexin-B1 within the cell remain unknown. I believe my work will help to uncover an important mechanism for tumor-induced angiogenesis, thereby presenting new targets for the development of anti-angiogenic therapy for oral cancer.
Publications:
Sun Q., Zhou H., Binmadi N., Basile J.: Hypoxia inducible factor-1-mediated regulation of Semaphorin 4D affects tumor growth and vascularity. J Biol Chem 2009 Sep 17. [Epub ahead of print]
Sun Q., Nawabi-Ghasimi F., Basile J.: Semaphorins in vascular development and head and neck squamous cell carcinoma-induced angiogenesis. Oral Oncol 2008 June; 44(6):523-31.
Basile J., Gavard J., Gutkind J.S.: Plexin-B1 Utilizes RhoA and ROK to Promote the Integrin-dependent Activation of AKT and ERK, and Endothelial Cell Motility. J Biol Chem 2007 Nov 30; 282(48): 34888-95.
Basile J., Holmbeck K., Bugge T.H., Gutkind J.S.: MT1-MMP Controls Tumor-Induced Angiogenesis through the Release of Semaphorin 4D. J Biol Chem 2007 Mar 2; 282(9): 6899-905.
Basile J., Castilho R.M., Williams V.P., Gutkind J.S.: Semaphorin 4D Provides a Link between Axon Guidance Processes and Tumor-Induced Angiogenesis. Proc Natl Acad Sci U S A 2006 Jun 13; 103(24): 9017-22.
Basile J., Afkhami T., Gutkind J.S.: Semaphorin 4D-Mediated Activation of Plexin-B1 Induces Endothelial Cell Migration Through Activation of PYK2, Src and the PI3K-Akt pathway. Mol Cell Biol 2005; 25: 6889-98.
Basile, J., Barac, A., Zhu, T., Guan, K., and Gutkind, J.S.: Class IV Semaphorins promote angiogenesis by stimulating Rho-initiated pathways through Plexin-B. Ca Res 2004 Aug 1; 64: 5212-24.
Basile, J., Eichten, A., Zacny, V., and Münger, K.: NF-kappa B-mediated induction of p21Cip1/Waf1 by tumor necrosis factor alpha induces growth arrest and cytoprotection in normal human keratinocytes. Molecular Cancer Research 2003 February; 1: 262-70.
Münger, K., Basile, J., Duensing, S., Eichten, A., Gonzalez, S., and Zacny, V.: Biological activities and molecular targets of the human papillomavirus E7 oncoprotein. Oncogene 2001 November 26; 20(54): 7888-98.
Basile, J., Zacny, V., Munger, K.: The cytokines TNF-alpha and TRAIL differentially modulate proliferation and apoptotic pathways in human keratinocytes expressing the HPV-16 E7 oncoprotein. J Biol Chem 2001 June 22; 276(18): 22522-8.
Duensing, S., Lee, L., Duensing, A., Basile, J., Piboonniyom, S., Gonzalez, S., Crum, C., and Münger, K.: The human papillomavirus type 16 E6 and E7 oncoproteins cooperate to induce mitotic defects and genomic instability by uncoupling centrosome duplication from the cell division cycle. Proc Natl Acad Sci USA 2000 Aug 29; 97(18): 10002-7.
