My research has been focused on the regulation of RTK signaling pathways by the Sprouty (Sprys) family of proteins and Sef (similar expression to FGF, or IL17rd), which play critical roles in cell proliferation, differentiation, survival and apoptosis. The overall goal of our study is to apply our knowledge of basic signaling mechanisms to human disease including cardiovascular and bone diseases. Over the past years, we have developed gain- and loss-of Sprys or Sef transgenic mice, and found that Sprys and Sef as RTK signaling modulators play crucial roles in cardiovascular and bone development and homeostasis. Recently, we are interested in how Sprys and Sef function and the mechanisms in the pathology of cardiovascular and bone. We believe our studies will have implication in developing strategies for fighting cardiovascular and bone diseases.
A side project of my research is to better understand the regulation of mammary gland development and homeostasis, and breast cancer initiation, progression and metastasis. My focus is whether Spry1 has roles, and what mechanisms of Spry1 functions in mammary gland development and breast cancer, and with emphasis on how Spry1 regulates the interactions of stromal-epithelial, myoepithelial-luminal epithelial cells, and how Spry1 regulates MaSC maintenance and differentiation.
The proper reciprocal interactions of stromal-epithelial, and basal-luminal epithelial cells are required for normal mammary development, and continuous remodeling during female reproductive cycles. Abnormalities in these interactions play an important role throughout different stages of breast carcinogenesis. The information gained from the proposed studies will advance our understanding of mammary gland morphogenesis and homeostasis, and will likely shed new sight on how breast cancer cells arise and progress.
A complete list of publications can be found on MyNCBI
He Q, Jing H, Liaw L, Gower L, Vary C, Hua S, Yang X. 2015. Suppression of Spry1 inhibits triple-negative breast cancer malignancy by decreasing EGF/EGFR mediated mesenchymal phenotype. Scientific Reports. In revision.
Yang X, Liaw L, Prudovsky I, Brooks PC, Vary C, Oxburg L, Friesel R. 2015. Fibroblast growth factor signaling in the vasculature. Curr Atheroscler Rep, 17(6):509.
He Q, Yang X, Gong Y, Canalis E, Rosen C, Friesel R. 2014. Deficiency of Sef in mice is associated with increased postnatal bone mass. JBMR, 29(5): 1237-31.
Gong Y, Yang X, He Q, Gower L, Brooks P, Vary C, Friesel R. 2013. Sprouty4 regulates endothelial cell migration via modulating integrin b3 stability through c-Src. Angiogenesis. 16(4):861-75.
Yang X*, Gong Y, Tang Y, Li H, He Q, Gower L, Liaw L, Friesel R*. 2013. Spry1 and Spry4 differently regulate human aortic smooth muscle cell phenotype via Akt/FoxO/myocardin signaling. PLOS ONE. 8(3):e58746, *: co-correspond author.
Brown AC, Adams D, de Caestecher M, Yang X, Friesel R, Oxburgh L. 2011. FGF/EGF signaling regulates the renewal of early nephron progenitors during embryonic development. Development, 138(23): 5099-112.
Tang Y, Yang X, Vary C, Friesel R, Liaw L. 2011. Mechanisms of TGFb induced differentiation in human vascular smooth muscle cells. J of Vascular Research. 48(6): 485-494.
Yang X, Gong Y, Friesel R. 2011. Spry1 is expressed in hemangioblasts and negatively regulated primitive hematopoiesis and endothelial cell function. PLOS ONE. 6(4): e18374.
Urs S, Venkatesh D, Tang Y, Henderson T, Yang X, Friesel R, Rosen CJ and Liaw L. 2010. Spry1 is a critical regulator of mesenchymal stem cell lineage allocation. FASEB J. 24: 3264-3273.
Tang Y, Harrington A, Yang X, Friesel R, and Liaw L. 2010. The contribution of the Tie2 lineage to primitive and definitive hematopoietic cells. Genesis. 48(9): 563-7.