Jialing Xiang , Ph.D.
Associate Professor of Biology
Office: 396 Life Sciences Building
Phone: 312.567.3491
Fax: 312.567.3494
Email: xiang@iit.edu
Expertise
- Molecular cell biology
- Signal transduction and programmed cell death in cancer cells
Education
- M.D. Xuzhou Medical College
- Ph.D. University of Alabama at Birmingham
Curriculum Vitae
Research & Major Accomplishments
The work in my laboratory is focused on the signaling network of cancer and its potential therapy. Cancer is characterized by uncontrolled cell growth, which results from unlimited proliferation and malfunction of programmed cell death (apoptosis). It is recognized that apoptosis plays a critical role in the development and progression of cancer. The apoptotic process is regulated by many genes, including the Bcl-2 family. The Bcl-2 family contains pro-apoptotic molecules such as Bax and Bak, and anti-apoptotic molecules such as Bcl-2 and Bcl-xL. We use the pro-apoptotic Bax molecule as a model system to study the role of the apoptotic signalings and its cross-talk with other survival signaling pathways in cancer cells. We are currently studying the Bax-mediated apoptotic pathway and its associated signal-transduction network in the progression of prostate cancer using both in vitro and in vivo prostate cancer model systems. We believe that understanding the apoptotic signaling mechanism of cancer cells should shed light on our understanding of cancer development and may provide information critical for treatment and prevention of cancers.
Current Projects
Awards/Honors
Patents
Books
Selected Publications
Godfrey B, Lin Y, Larson J, Haferkamp B, Xiang J. (2010). Stress-induced proteasomaldegradation unleashes the pro-death activity of androgen receptor. Cell Res. 20: 1138-1140.
Tang F, Kokontis J, Lin Y, Liao S, Lin A, Xiang, J. (2009).Androgen via p21 inhibits TNFalpha-induced JNK activation and apoptosis. J Biol Chem. 284(47):32353-8.
Deng, H., Yu, F., Chen, J., Zhao, Y., Xiang, J., Lin, A. (2008). Phosphorylation of bad at Thr201 by JNK1 promotes glycolysis through activation of phosphofructokinase-1. J. Biol.Chem. 283(30):20754-60.
Lin, Y., Fukuchi, J., Hiipakka, R., Kokontis, J., and Xiang, J. Up-regulation of Bcl-2 is required for the progression of prostate cancer cells from androgen-dependent to androgen-independent growth. Cell Res. 17(6), 531-536 (2007).
Lin, Y., Kokontis, J., Tang, F., Liao, S., Lin, A., Chen, C., and Xiang, J. Androgen and Its Receptor AR Promote BAX-mediated Apoptosis. Mol. Cell. Biol. 26(5), 1908 –1916 (2006).
Yu, C., Minemoto, Y., Zhang, J., Liu, J., Tang, F., Bui, T., Lin, A.* and Xiang, J*. Activation of the JNK pathway inhibits IL-3 withdrawal induced apoptosis in B-lymphocytes. Molecular Cell. 13, 329-340 (2004).
Xiang, J., Gomez-Navarro, J, Arafat, W., Liu B., Barker, S.D., Alvarez, R.D., Siegal G.P., and Curiel, D.T. Pro-apoptotic treatment with an adenovirus encoding bax enhances the effect of chemotherapy in ovarian cancer. J. Gene Medicine 2(2), 97-106 (2000).
Xiang, J., Chao, D.T., and Korsmeyer, S.J. Bax-induced cell death may not require interleukin 1 b-converting enzyme-like proteases. Proc. Natl. Acad. Sci. USA. 93, 14559-14563 (1996).
