Li Xin, Ph.D.
Department of Molecular and Cellular Biology
Ph.D.: Shanghai Institute of Biochemistry and Cellular Biology, Chinese Academy of Sciences, Shanghai, China
Postdoctoral training: University of California, Los Angeles
Prostate Biology and Prostate Carcinogenesis
My lab is interested in using the prostate as a tissue model to study the molecular and cellular mechanisms that regulate development, tissue homeostasis and carcinogenesis. Currently, there are two major research focuses in the lab. The first research focus is to characterize the prostate epithelial lineage hierarchy. We seek to investigate how individual prostate epithelial lineages are maintained in adults by prostate stem cells or progenitors, and to identify master regulators that control adult prostate homeostasis. The second focus of the lab is to investigate the molecular and cellular basis of aggressive prostate cancer. We are interested in determining the function of disease-associated genes in prostate cancer initiation and progression, and characterizing the identity of the cells of origin for prostate cancer.
The major approaches that we utilize are cell culture-based prostate stem cell assays, genetically engineered mouse models, and a prostate regeneration method. In the prostate regeneration assay, FACS-isolated prostate stem/progenitor cells from adult mice are mixed with embryonic urogenital sinus mesenchymal cells (UGSM) and grafted under the kidney capsules of immunodeficient mice. Stem/progenitor cells are stimulated by the UGSM cells to reconstitute tissues reminiscent of the prostate. In this system, both epithelial and mesenchymal cells can be efficiently infected with lentivirus that enable expression of genes of interest, which enables us to study gene action in specific cell lineages in a much faster way than the traditional transgenic approach.
Prostate cancer is the second leading cause for cancer-related death in men in the United States. Research in my lab will help solve some of the major therapeutic challenges for prostate cancer, such as distinguishing indolent prostate cancers from aggressive ones that need immediate therapeutic intervention.
Baylor College of Medicine
One Baylor Plaza, DeBakey, M533A
Houston, TX 77030
- Valdez JM, Zhang L, Su QT, Dakhova O, Zhang Y, Shahi P, Spencer DM, Creighton CJ, Ittmann M, Xin L. (2012). Notch and TGFβ form a reciprocal positive regulatory loop that suppresses murine prostate basal stem/progenitor cell activity. Cell Stem Cell. In Press
- Choi N, Zhang BY, Zhang L, Ittmann M, Xin L. (2012). Adult murine prostate basal and luminal cells are self-sustained lineages that can both serve as targets for prostate cancer initiation. Cancer Cell 21(2), 253-265.
- Zhang L, Valdez JM, Zhang BY, Chang J, Lei W, Xin L. (2011). ROCK inhibitor Y-27632 suppresses dissociation-induced apoptosis of murine prostate basal stem/progenitor cells and increases their cloning efficiency. PLoS One 2011 Mar 28;6(3):e18271.
- Shahi P, Seethammagari MR, Valdez JM, Xin L, Spencer DM.(2011). Wnt and Notch pathways have interrelated opposing roles on prostate progenitor cell proliferation and differentiation. Stem Cells 2011; Feb 3.
- Zhang L, Zhang BY, Valdez JM, Wang F, Ittmann M and Xin L. (2010). Dicer ablation impairs prostate stem cell activity and causes prostate atrophy. Stem Cells 2010; July. 28(7): 1260-9.
- Zong Y, Xin L, Goldstein A, Lawson D, Teitell M and Witte ON. (2009). Alternative cooperating events in the progression of ERG-initiated prostate cancer. Proc Natl Acad Sci U S A. 2009 July 28:106(30).
- Memarzadeh S, Xin L, Mulholland D, Teitell MA, Wu H and Witte ON. (2007). Enhanced paracrine FGF10 expression promotes formation of multifocal prostate adenocarcinoma and an increase in epithelial androgen receptor. Cancer Cell. V12, 572-85.
- Xin L, Lukacs RU, Lawson DA, Cheng D and Witte ON. (2007). Self renewal and multilineage differentiation in vitro from murine prostate stem cells. Stem Cells. 25(11) 2760-69.
- Xin L, Teitell, MA, Lawson DA, Kwon, A, Mellinghoff, IK, Witte ON. (2006). Progression of prostate cancer by synergy of AKT with genotropic and non-genotropic actions of the androgen receptor. Proc Natl Acad Sci U S A. 103(20);7789-94.
- Xin L, Lawson DL, Witte ON. (2005). The Sca-1 cell surface marker enriches for a prostate stem/progenitor cell subpopulation that can initiate prostate tumorigenesis. Proc Natl Acad Sci U S A. 2005 May 10;102(19):6942-7.