Welcome to the Hussaini Lab

Welcome to the Hussaini Lab

UVA Rotunda - Hussaini Lab

The research in my laboratory is centered on understanding the basic cellular mechanisms involved in astrocytoma invasive growth. The prognosis for patients with malignant astrocytomas tumors (brain tumors) is poor. The capacity of astrocytomas both to invade adjacent brain sites and to migrate to distant ones precludes curative surgical resection; and little progress has been made in designing adjuvant therapies that significantly affect long-term patient survival. In order to formulate more novel therapeutic strategies, it is essential to have a better understanding of how the invasive growth of these tumors is controlled.

The primary interest of the laboratory is the regulation of LRP (low density lipoprotein receptor-related protein) expression and function in astrocytic tumor cells. LRP is an endocytic receptor involved in the trafficking of a variety of protein/protein complexes {including urokinase (uPA) and its receptor (uPAR), Lipoprotein metabolites, and activated alpha2-macroglobulin} that have patho- physiologic relevance in the central nervous system tumors. Alteration in LRP expression regulates the levels of modulators (uPA, uPAR and PAI-1) of migration/invasion around the microenvironment of astrocytic tumors (Funded by National Institute of Neurological Disorders and Stroke, NIH from 1997-2008).

The second project in my laboratory focuses on understanding differences in PKC-eta activation and expression between malignant vs. non-neoplastic astrocytes and on the role of PKC-eta in the control of cell proliferation and apop- tosis. The regulation of cell proliferation and apoptosis in malignant astrocytic tumors is undoubtedly complex; however, we are investigating how PKC-eta regulation of these processes may be exploited to provide an experimental system in which proliferative or apoptotic phenotype may be selectively induced and studied. We are also extrapolating some of our results in cultured cells to glioblastoma animal models in collaboration with Dr. Mark Shaffrey (Department of Neurological Surgery). We hypothesize that pharmacological regulation of PKC-eta, in combination with drugs targeting cellular migration, may present a new therapeutic paradigm for these aggressive brain tumors (Funded by National Cancer Institute, NIH from 2002-2007).


1. Hussaini IM, Sando JJ, Shaffrey ME, VandenBerg SR. Protein kinase C-eta regulates resistance to UVA- and y-irradiation-induced apoptosis by preventing caspase-9 cleavage in astrocytomas. Neuro-Oncology 2002; 4(1):9-13. Link to Paper (PDF)

2. Goldfarb AN, Delehanty LL, Wang D, Facke FKE, Hussaini IM. Stromal inhibition of megakaryocytic differentiation correlates with blockade of signaling b protein kinase C-epsilon and ERK/MAPK. J Biol Chem 2001; 276(31):29526-29530. Link to Paper (PDF) Link to Paper (HTML)

3. Hussaini IM, Karns LR, Griffith V, Carpenter JE, Redpath GT, Sando JJ, VandenBerg SR. Phorbol 12-Myristate-13-Acetate induces protein kinase C-eta-specific proliferative response in astrocytic tumor cells. J. Biol. Chem. 2000; 275(29):22348-22354. Link to Paper (PDF) Link to Paper (HTML)

4. Hussaini IM, Karns LR, Redpath GT, Carpenter J, Gonias SL, Vandenberg SR: Epidermal growth factor receptor ligands induce transcriptional down-regulation of low density lipoprotein receptor-related protein (LRP) gene expression in human glioblastoma cells. Glia 1999; 25: 71-84. Link to Paper (PDF)

Five research area designations: (1) Tumor Biology, (2) Signal Transduction (3) Cell Migration and Invasion, (4) Apoptosis, and (5) Cell and Molecular Biology.