Xiuwei Yang, Ph.D.

Bio / Education: 

Dr. Yang studies revolve around the role of the extracellular matrix in breast cancer. He recently received an institutional grant from the American Cancer Society to determine whether macrophage-mediated malignancy in breast cancer is mediated via extracellular proteins known as integrins.

Research Description: 

The primary research interest of our laboratory is to understand how cell adhesion molecules or receptors contribute to cancer development, progression and metastasis, and to evaluate the potential of these molecules as candidate biomarkers or therapeutic targets for the early detection, diagnosis and treatment of such malignant diseases. Our recent projects involve the functional analyses of heterodimeric adhesion receptors, named laminin-binding (LB) integrins (i.e., alpha3/beta1, alpha6/beta1 and alpha6beta4, and their associated tetraspanin CD151, in human breast, ovarian and skin cancer as well as mammary gland development. In these studies, we have attempted to assess tumor onset and metastasis as well as underlying mechanisms by using gene-targeted mice, transgenic animal models and 3D cell culture model. Our current studies focus on the following functional aspects of these molecules and their associated protein complexes:

• Signaling roles in tumor cell proliferation, motility and invasion in multiple types of human carcinomas
• Genetic and transcriptional regulation of the niches and homeostasis of normal or malignant epithelial stem/progenitor cells
• Control of the reciprocal interactions between tumor cells and their microenvironments (e.g., remodeling of extracellular matrices and infiltration of stroma cells)
• Transcriptional regulation of cell-cell contacts and Epithelial-Mesenchymal Transition (EMT) during tumor progression
• Molecular contribution to late-stage tumor metastasis, e.g., tumor cell extravasation through vasculature or colonization at distant sites.
• Collaboration with diverse oncogenic or pro-malignant pathways, including those driven by Receptor Tyrosine Kinases (e.g., EGFR and ErbB2), focal adhesion kinase (FAK) and small GTPases (Rac1, Rho A and Cdc42), as well as canonical Wnt signaling.

PubMed Publications: