Department of Cell Biology & Molecular Medicine
Lizhao Wu, Ph.D.
Ph.D. in Molecular Genetics, The Ohio State University
Postdoc in Mouse Genetics and Cancer Genetics, The Ohio State University Comprehensive Cancer Center
Major Awards & Achievements
2003 Howard Temin Career Development Award, NCI/NIH
2000 Postdoctoral Fellowship in Oncology, NIH
1997 Presidential Fellowship, Ohio State University
1997 Graduate School Alumni Research Award, Ohio State University
1989 Advancement in Sciences and Technology, Chinese Department of Agriculture
Awards from Lab Members
Two members from the lab received a Postdoctoral Fellowship from NJCCR (Dr. T. Hu in 2009 and Dr. Tome-Garcia in 2012). Three members received the Gallo Award from NJCCR and CINJ (Dr. T. Hu in 2008 & 2009, Dr. S. Ghazaryan and Ms. D. Li in 2011).
Lizhao Wu, Ph.D.
Research: My laboratory is primarily interested in understanding how the Rb/E2F pathway and other tumor suppressor/oncogenic pathways control normal development and cancer.
Seda Ghazaryan, PhD
Ph.D., 1999, Ohio State University, Dept. of Molecular Genetics, Columbus, Ohio, Molecular Genetics
|Wu, L., C. Timmers, B. Maiti, H. I. Saavedra, L. Sang, G. T. Chong, F. Nuckolls, P. Giangrande, F. A. Wright, M. E. Greenberg, S. Orkin, J. R. Nevins, M. L. Robinson, and G. Leone, 2001. The E2F1, E2F2, and E2F3 transcription factors are essential for cellular proliferation. Nature 379: 457-462.|
|Saavedra, H. I., L. Wu, A. de Bruin, C. Timmers, T. J. Rosol, M. Weinstein, M. L. Robinson, and G. Leone, 2002. Specificity of E2F1, E2F2 and E2F3 in mediating phenotypes induced by loss of Rb. Cell Growth Differ. 13: 215-225.|
|de Bruin, A., L. Wu, H. I. Saavedra, P. Wilson, Y. Yang, T. J. Rosol, M. Weinstein, M. L. Robinson, and G. Leone, 2003. Rb function in extraembryonic lineages suppresses apoptosis in the central nervous system of Rb-deficient mice. Proc. Natl. Acad. Sci. USA 100: 6546-6551.|
|Wu, L., A. de Bruin, H. I. Saavedra, M. Starovic, Y. Yang, A. Trimboli, J. Opavska, P. Wilson, M. C. Ostrowski, J. C. Cross, M. Weinstein, T. J. Rosol, M. L. Robinson, and G. Leone, 2003. Extra-embryonic function of Rb is essential for embryonic development and viability. Nature 421: 942-947 (Cover Highlight/News & Views 421: 903-904).|
|Zhang, J., J. Gray, L. Wu, G. Leone, S. Rowan, C. L. Cepko, X. Zhu, C. M. Craft, and M. A. Dyer, 2004. Rb regulates proliferation and rod photoreceptor development in the mouse retina. Nature Genet. 36: 351-360.|
|*Wenzel, P. L., *L. Wu, A. de Bruin, J. Chong, W. Chen, G. Dureska, E. Sites, T. Pan, A. Sharma, K. Huang, R. Ridgway, K. Mosaliganti, R. Sharp, R. Machiraju, J. Saltz, H. Yamamoto, J. C. Cross, M. L. Robinson, and G. Leone, 2007. Rb is critical in a mammalian tissue stem cell population. Genes Dev. 21: 85-97. (*Equal contributions)|
|Tsai, S., R. Opavsky, N. Sharma, L. Wu, S. Naidu, E. Nolan, E. Feria-Arias, C. Timmers, J. Opavska, A. de Bruin, J. Chong, P. Trikha, P. Stromberg, & G. Leone, 2008. Mouse development with a single E2F activator. Nature 454: 1137-1141.|
|Hu, T., S. Ghazaryan, C. Sy, C. Wiedmeyer, V. Chang, and L. Wu, 2012. Concomitant inactivation of Rb and E2f8 in hematopoietic stem cells synergizes to induce severe anemia. Blood, 119: 4532-4542 (highlighted as a University News Release by the University of Medicine and Dentistry of New Jersey News Service on July 13, 2012).|
|Wu, L.*, A. de Bruin*, H. Wang, T. Simmons, W. Cleghorn, L. E. Goldenberg, E. Sites, A. Sandy, A. Trimboli, S. A. Fernandez, C. Eng, C. Shapiro, and G. Leone. Selective roles of E2Fs for ErbB2- and Myc-mediated mammary tumorigenesis. Oncogene (in press) (Corresponding author)(*Equal contributions).|
|Ghazaryan, S., C. Sy, T. Hu, X. An, N. Mohandas, H. Fu, M. Aladjem, V. Chang, R. Opavsky, and L. Wu, 2014. Loss of Rb and E2f8 synergizes to trigger stressed DNA replication during erythroid terminal differentiation. Molecular and Cellular Biology 34(15): 2833-2847.|
Areas of Interest
Oncogene and tumor suppressor pathways in normal development and cancer
One of the hallmarks of cancer is uncontrolled cellular proliferation, which typically stems from acquired genetic or epigenetic alterations to genes that directly regulate the cell cycle. Particularly critical to the cell cycle control are the signals that regulate the passage of cells through the G1 phase into S phase. Numerous studies have led to the delineation of a pathway controlling the progression of cells out of quiescence, through G1, and into S phase that involves the activation of G1 cyclin-dependent kinases (CDKs), phosphorylation and inactivation of the retinoblastoma (Rb) and other pocket proteins, and the subsequent release of E2F transcription factors. It is now evident, from studies using both in vitro cell culture systems and in vivo mouse models, that the tumor suppressor function of Rb is partly mediated through its interaction with the E2F family and its regulation of E2F-dependent transcriptional activation or repression. Considering the central role of the Rb/E2F pathway in the control of cell cycle, it is not surprising that essentially all human malignancies analyzed so far contain genetic alterations in this pathway, either through the activation of positive acting components such as Ras, Myc, and G1-cyclins, or by the inactivation of negative cell cycle regulators such as Rb and CDK inhibitors. Importantly, increasing evidence also implicates various E2F transcription factors in regulating normal cellular proliferation and aberrant cell growth or cancer.
My laboratory is primarily interested in understanding how the Rb/E2F pathway and other tumor suppressor/oncogenic pathways control normal development and cancer. We will use both in vitro cell/tissue culture systems and in vivo mouse models to delineate various signaling networks in several model systems, including the hematopoietic system, the prostate glands, and the mammary glands. Our studies will not only provide critical insights on how various tumor suppressor and oncogenic signaling pathways function and interact, but may also lead to improved cancer diagnosis, prognosis, and molecule- or pathway-based cancer therapies.