Wei Li, PhD

Professor of Dermatology

Director, MSS Graduate Program

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Overview

Dr. Li research focuses on the following topics: 1) Identification of the “driver genes” for wound healing, 2) Identification of tumor-secreted molecules as drug targets for TNBCs (triple negative breast cancers). 3) Signal transduction to understand the cell motility signaling, which initiates at the cell surface, propagates via cytosolic signaling networks and executes by newly expressed and secreted gene products.

His experimental model systems are less manipulated primary human skin cells, whose migration is essential for both physiological processes, such as skin wound healing, and pathological occurrence, such as skin cancer, PDX models for TNBCs and pig models for wound healing.

Awards

  • USC Stevens Center for Innovation: Technology Commercialization Award, 2017
     – 2017
  • USC Stevens Center for Innovation: Technology Commercialization Award, 2018
     – 2018
  • USA: Elected Member, National Academy of Inventors, 2017
     – pre.

Education and Training

  • Xinjiang University, Urumqi, China — B.S. — 1982 — General Biology
  • CUSBEA, Guangzhou, China — English Certificate — 1984 — English
  • Albert Einstein College of Medicine, New York City, NY — Ph.D. — 1991 — Biochemistry and Molecular Biology
  • New York University Medical Center, New York City, NY — Postdoctoral Research — 1993 — Signal Transduction

Research Funding

  • Development of Extracellular Heat Shock Protein-90 as a Novel Topical Wound Healing
    NIH · R01AR059853 · Jul 1, 2011 – Apr 30, 2018 · Role: Principal Investigator
  • Mechanisms of Human Dermal Fibroblast Migration
    NIH · R01GM067100 · Jan 1, 2003 – Apr 30, 2021 · Role: Principal Investigator
  • Signal Transduction of Human Keratinocyte Migration
    NIH · R01GM066193 · Jul 1, 2002 – May 31, 2013 · Role: Principal Investigator
  • STUDIES OF A NOVEL SH2/SH3-CONTAINING CELLULAR ONCOGENE
    NIH · R01CA065567 · Aug 15, 1995 – Apr 30, 2001 · Role: Principal Investigator

Research Keywords

  • big molecule drug development, wound healing, breast cancer

Publications

  • Extracellular Hsp90 (eHsp90) as the actual target in clinical trials: intentionally or unintentionally. Int Rev Cell Mol Biol. 2013; 303:203-35.. View in PubMed
  • The anti-motility signaling mechanism of TGFβ3 that controls cell traffic during skin wound healing. Biol Open. 2012 Dec 15; 1(12):1169-77.. View in PubMed
  • A potentially common peptide target in secreted heat shock protein-90α for hypoxia-inducible factor-1α-positive tumors. Mol Biol Cell. 2012 Feb; 23(4):602-13.. View in PubMed
  • A fragment of secreted Hsp90α carries properties that enable it to accelerate effectively both acute and diabetic wound healing in mice. J Clin Invest. 2011 Nov; 121(11):4348-61.. View in PubMed
  • Secreted heat shock protein-90 (Hsp90) in wound healing and cancer. Biochim Biophys Acta. 2012 Mar; 1823(3):730-41.. View in PubMed
  • TbetaRI/Alk5-independent TbetaRII signaling to ERK1/2 in human skin cells according to distinct levels of TbetaRII expression. J Cell Sci. 2011 Jan 01; 124(Pt 1):19-24.. View in PubMed
  • Participation of the lipoprotein receptor LRP1 in hypoxia-HSP90alpha autocrine signaling to promote keratinocyte migration. J Cell Sci. 2009 May 15; 122(Pt 10):1495-8.. View in PubMed
  • Characterization of molecular mechanisms underlying mutations in dystrophic epidermolysis bullosa using site-directed mutagenesis. J Biol Chem. 2008 Jun 27; 283(26):17838-45.. View in PubMed
  • Transforming growth factor alpha (TGFalpha)-stimulated secretion of HSP90alpha: using the receptor LRP-1/CD91 to promote human skin cell migration against a TGFbeta-rich environment during wound healing. Mol Cell Biol. 2008 May; 28(10):3344-58.. View in PubMed
  • Extracellular heat shock protein-90alpha: linking hypoxia to skin cell motility and wound healing. EMBO J. 2007 Mar 07; 26(5):1221-33.. View in PubMed