Fei Liu, PhD
Education and Post-Graduate Training
Dr. Fei Liu received his Bachelor of Clinical Medicine (equivalent to MD) and a Master of Medical Immunology from the 4th Military Medical University of China in 1995 and 1998, respectively. He received his PhD in molecular immunology from the 4th Military Medical University in 2002 working with Dr. Boquan Jin on signal transduction of Interleukin-6 family cytokines and Notch pathway. His postdoctoral work was at the University of Dundee and University of Aberdeen in Scotland in the laboratory of Dr. Stefan Hoppler. His research focused on the molecular mechanism that determines tissue-specific responses to Wnt signaling, then in 2005 he accepted a position at the University of Pennsylvania in Dr. Sarah Miller’s lab continuing his Wnt signaling research in development of epithelial appendages. Dr Liu joined the faculty at the Texas A&M University Health Science Center in October 2008.
Roles of mesenchymal stem cells (MSCs) in growth and metastasis of cancer and application of MSCs for cancer treatment
MSCs are an essential source of cancer-associated fibroblasts (CAFs) that promote growth and metastasis of cancers. On the other hand, the tumor-tropic property makes MSCs a promising vehicle for gene-therapy
of cancers. Liu’s recent work indicated that Transforming growth factor (TGF-?) pathway is essential for differentiation of MSCs into CAFs and the interaction between MSCs and cancer cells, which suggested
that blocking TGF-? pathway would significantly improve the safety of MSCs-mediated therapies in cancer patients. Meanwhile, blocking TGF-? pathway in MSCs also disrupted the cytokine network essential for maintenance
of breast cancer stem cells. Liu’s current works are on MSC mediated disruption of niches for breast cancer stem cells and metastasis.
Molecular cues for regeneration of salivary glands.
Salivary gland destruction is a major consequence of various pathological conditions such as radiation therapy for head and neck cancer and Sjögren’s syndrome. Dry mouth syndrome severely compromises
quality of life in these patients, while currently available treatments cannot restore salivary gland functions. Stem cells based regenerative therapy is a promising direction to treat this condition. Liu’s
work revealed for the first time that Wnt (wingless/int) and Hedgehog signaling promote expansion of salivary gland stem cells. Transient activation of Wnt signaling prevented radiation-induced hypo-salivation
by prevention of apoptosis but can’t rescue it. Transient activation of Hedgehog pathway rescued radiation-induced hypo-salivation by perseveration of functional salivary stem/progenitor cells and innervation.
The molecular mechanisms of Hedgehog-mediated rescue effects are under investigation.
Molecular cues for development and regeneration of tooth root/periodontal tissues.
From the clinical point of view, root/periodontal tissues (R/PT) are the most important part of teeth, which provide support and fixture for natural or artificial crowns and are not replaceable with current technologies. It's believed that like the development of tooth crown, the formation of R/PT also requires sequential and reciprocal interaction between dental epithelia and mesenchyme mediated by protein messengers known as signaling molecules. Liu’s recent work revealed that interaction between Bone Morphogenetic Protein (BMP) and Wnt pathways determine the fate of dental epithelia both collaboratively and antagonistically. This project will provide essential data for understanding the complex molecular control of this process, and clues for designing new strategies to build up a bio-root/periodontal complex in cases of tooth loss due to disease or trauma.
Graduate training is available through the Medical Science PhD program (College of Medicine), through the MD/PhD program(College of Medicine) and other programs that our faculty are affiliated with joint research.
- Qingguo Zhao, Carl A. Gregory, Ryang Hwa Lee, Roxanne L. Reger, Lizheng Qin, Bo Hai, Min Sung Park, Nara Yoon, Bret Clough, Eoin McNeill, Darwin J. Prockop, and Fei Liu. MSCs derived from iPSCs with a modified protocol are tumor-tropic but have much less potential to promote tumors than bone marrow MSCs. Proc Natl Acad Sci U S A. 2015 Jan 13;112(2):530-5. doi: 10.1073/pnas.1423008112. PMID: 25548183. http://www.ncbi.nlm.nih.gov/pubmed/25548183
- Bo Hai, Lizheng Qin, Zhenhua Yang, Qingguo Zhao, Lei Shangguan, Xinyu Ti, Yanqiu Zhao, Sangroh Kim, Dharanipathy Rangaraj, and Fei Liu. Transient Activation of Hedgehog Pathway Rescued Radiation-induced Hyposalivation. Clinical Cancer Research, 2014 Jan 1;20(1):140-50. doi:10.1158/1078-0432.CCR-13-1434. http://www.ncbi.nlm.nih.gov/pubmed/24150232
- Zhenhua Yang, Bo Hai, Lizheng Qin, Xinyu Ti, Lei Shangguan, Yanqiu Zhao, Lindsey Wiggins, Ying Liu, Jian Q. Feng, Julia Yu Fong Chang, Fen Wang, Fei Liu. Cessation of epithelial Bmp signaling induces formation of cementum-like structures on tooth crowns by promoting EMT in a Wnt-dependent manner. Molecular and Cellular Biology, 2013. Dec;33(23):4732-44. doi: 10.1128/MCB.00456-13. Cover feature. http://www.ncbi.nlm.nih.gov/pubmed/24081330
- Lei Shangguan, Xinyu Ti, Ulf Krause, Bo Hai, Yanqiu Zhao, Zhenhua Yang, and Fei Liu. Inhibition of TGF-β/Smad signaling by BAMBI blocks differentiation of human mesenchymal stem cells to carcinoma-associated fibroblasts and abolished their pro-tumor effects. Stem Cells, 2012 Dec;30(12):2810-9. doi: 10.1002/stem.1251. http://www.ncbi.nlm.nih.gov/pubmed/23034983
- Bo Hai, Zhenhua Yang, Lei Shangguan, Yanqiu Zhao, Arthur Boyer and Fei Liu. Concurrent Transient Activation of Wnt/β-catenin Pathway Prevents Radiation Damage to Salivary Glands. International Journal of Radiation Oncology*Biology*Physics (IJROBP). 2012 May 1;83(1):e109-16. http://www.ncbi.nlm.nih.gov/pubmed/22342093
- Bo Hai, Zhenhua Yang, Yeon Sook Choi, Sarah E. Millar, Makoto Mark Taketo, Andras Nagy, and Fei Liu. Wnt/β-catenin signaling regulates postnatal development and regeneration of the salivary gland. Stem Cells and Dev. 2010 19(11): 1793-1801. Cover feature. http://www.ncbi.nlm.nih.gov/pubmed/20367250