Xiaojie Ma
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Research Interests
Xiaojie Ma has a total of 6 co-authors. Here are the top co-authors by number of shared publications:
- Angelica Trujillo
† Department of Surgery, University of Florida, 1600 SW Archer Road, Gainesville, Florida 32610
1 shared publication - Carl Nyberg
† Department of Surgery, University of Florida, 1600 SW Archer Road, Gainesville, Florida 32610
1 shared publication - Elizabeth A. Beierle
Division of Pediatric Surgery, Department of Surgery, University of Alabama at Birmingham, Birmingham, AL 35233, USA
1 shared publication - Jerry E. Stewart
Division of Pediatric Surgery, Department of Surgery, University of Alabama at Birmingham, Birmingham, AL 35233, USA
1 shared publication - Vita M. Golubovskaya
Department of Surgical Oncology, Roswell Park Cancer Institute, Buffalo, NY 14263, USA
1 shared publication - William G. Cance
Department of Surgical Oncology, Roswell Park Cancer Institute, Buffalo, NY 14263, USA
1 shared publication
Latest Publications
- 1 March 2010
- Published by Taylor & Francis in Cell Cycle
- Vol. 9 (5) , 1005-1015
Inhibition of focal adhesion kinase decreases tumor growth in human neuroblastoma
Neuroblastoma is the most common extracranial solid tumor of childhood. Focal adhesion kinase (FAK) is an intracellular kinase that regulates both cellular adhesion and apoptosis. FAK is overexpressed in a number of human tumors including neuroblastoma. Previously, we have shown that the MYCN oncogene, the primary adverse prognostic indicator in neuroblastoma, regulates the expression of FAK in neuroblastoma. In this study, we have examined the effects of FAK inhibition upon neuroblastoma using a small molecule [1,2,4,5-benzenetetraamine tetrahydrochloride (Y15)] to inhibit FAK expression and the phosphorylation of FAK at the Y397 site. Utilizing both non-isogenic and isogenic MYCN+/MYCN- neuroblastoma cell lines, we found that Y15 effectively diminished phosphorylation of the Y397 site of FAK. Treatment with Y15 resulted in increased detachment, decreased cell viability and increased apoptosis in the neuroblastoma cell lines. We also found that the cell lines with higher MYCN are more sensitive to Y15 tr...
- 1 March 2010
- Published by Taylor & Francis in Cell Cycle
- Vol. 9 (5) , 1005-1015
Inhibition of focal adhesion kinase decreases tumor growth in human neuroblastoma
Neuroblastoma is the most common extracranial solid tumor of childhood. Focal adhesion kinase (FAK) is an intracellular kinase that regulates both cellular adhesion and apoptosis. FAK is overexpressed in a number of human tumors including neuroblastoma. Previously, we have shown that the MYCN oncogene, the primary adverse prognostic indicator in neuroblastoma, regulates the expression of FAK in neuroblastoma. In this study, we have examined the effects of FAK inhibition upon neuroblastoma using a small molecule [1,2,4,5-benzenetetraamine tetrahydrochloride (Y15)] to inhibit FAK expression and the phosphorylation of FAK at the Y397 site. Utilizing both non-isogenic and isogenic MYCN+/MYCN- neuroblastoma cell lines, we found that Y15 effectively diminished phosphorylation of the Y397 site of FAK. Treatment with Y15 resulted in increased detachment, decreased cell viability and increased apoptosis in the neuroblastoma cell lines. We also found that the cell lines with higher MYCN are more sensitive to Y15 tr...