Yayun Liang, PhD
Research Assistant ProfessorOffice Location: 133C Dalton Cardiovascular Research Center
Office Phone: 573-884-8116
liangya@missouri.edu
Research Interests
Research Description
The concept of specific molecular targeting has been applied to the development of innovative cancer-treatment strategies. At present, two main approaches are available for use in clinical practice: therapeutic monoclonal antibodies and small-molecule agents. Both antibodies and small-molecule compounds are therefore promising tools for target-protein-based cancer therapy. Mutations in p53 or the p53 pathway are thought to play a key role in promoting tumor cell survival and tumor cell resistance to chemotherapeutic drugs. Therefore restoring p53 function in tumors has been pursued as a promising strategy for cancer therapy. Furthermore, Tumor cell survival, growth, and metastasis require persistent blood vessel growth or angiogenesis. A tumor cannot grow beyond the size of about 1mm in diameter without acquiring new blood vessels to nurture it. Hence, targeting tumor blood vessels and tumor angiogenesis has been as a new strategy for treatment cancer. The aims of Liang's research are to 1) Develop innovative cancer-treatment strategies targeting mut-p53, tumor angiogenesis, and tumor blood vessels with novel antibodies and small molecules in advanced breast cancer models; 2) Define molecular signaling pathways involved in inhibition of tumor angiogenesis and induction of tumor cell apoptosis; and (c) Define the role of VEGF in tumor angiogenesis, growth, metastasis, and drug resistance.
Professional Background
- Obtained PhD in pharmacology, Beijing Medical University (Present: Health Science Center, Peking University), Beijing, China, October 1981.
- Obtained PharmD, Beijing Medical University (Present: Health Science Center, Peking University) Beijing, China, March 1976.
Selected Publications
- Liang Y, Besch-Williford C, Brekken R.A., and Hyder, S.M. Progestin-dependent progression of human breast tumor xenografts: a novel model for evaluating anti-tumor therapeutics. Cancer Research 67: 9929-9936, 2007.
- Liang Y, Besch-Williford C, Benakanakere I, and Hyder, S.M. Activation of p53 pathway suppresses proliferation of hormone-dependent human breast cancer cells in vitro and in vivo. Int J Oncol. 31: 777-784, 2007.
- Liang Y, Brekken R.A., and Hyder, S.M. Vascular endothelial growth factor induces proliferation of breast cancer cells and inhibits the anti0proliferative activity of anti-hormones. End Related Cancer 13: 905-919, 2006.
- Liang Y and Hyder, S. M. Proliferation of endothelia and tumor epithelial cells by progestin-induced VEGF from human breast cancer cells: Paracrine and Autocrine effects. Endocrinology 146: 3632-3641, 2005.
- Liang Y, Wu J. and Hyder, S. M. p53-dependent inhibition of progestin- Induced VEGF expression in human breast cancer cells. Journal of Steroid Biochemistry and Molecular Biology 93: 173-182, 2005.
- Liang Y, Eid, A. M, EL Etreby, Lewis R.W., and Kumar, VJ. Mitochondria from TRAIL- resistant prostate cancer cells are capable of responding to apoptotic stimuli. Cellular Signaling, 17: 243-251, 2005.
- Liang Y, Hou M, Kallab A.M., Barrett, J.T., EL Etreby, F., and Schoenlein P.V. Induction of antipriliferation and apoptosis in estrogen receptor negative MDA- 231 human breast cancer cells by mifepristone and 4- hydroxytamoxifun combination therapy: A role for TGFB International Journal of Oncology 23(2): 369-380, 2003.
- Liang Y, EL Etreby M.F., Lewis R.W., and Kumar, VJ. Mifepristone-induced secretion of Transforming Growth Factor-B1-induced apoptosis in prostate cancer cells. International Journal of Oncology 21: 1259-1267, 2002.