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Wei Li, PhD

Title(s)Professor of Dermatology
Phone+1 323 865 0618
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    Other Positions
    Title(s)Director, MSS Graduate Program


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    Collapse Education and Training
    Xinjiang University, Urumqi, ChinaB.S.1982General Biology
    CUSBEA, Guangzhou, ChinaEnglish Certificate1984English
    Albert Einstein College of Medicine, New York City, NYPh.D.1991Biochemistry and Molecular Biology
    New York University Medical Center, New York City, NYPostdoctoral Research1993Signal Transduction
    University of Chicago, Chicago, ILAssistant Professor1993-99Cancer Biology
    University of Southern California, Los AngelesProfessor1999-Wound Healing and Tumor Biology

    Collapse Overview 
    Collapse 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.

    Collapse Research 
    Collapse Research Activities and Funding
    Development of Extracellular Heat Shock Protein-90 as a Novel Topical Wound Healing
    NIH/NIAMS R01AR059853Jul 1, 2011 - Apr 30, 2016
    Role: Principal Investigator
    Mechanisms of Human Dermal Fibroblast Migration
    NIH/NIGMS R01GM067100Jan 1, 2003 - Apr 30, 2021
    Role: Principal Investigator
    Signal Transduction of Human Keratinocyte Migration
    NIH/NIGMS R01GM066193Jul 1, 2002 - May 31, 2013
    Role: Principal Investigator
    STUDIES OF A NOVEL SH2/SH3-CONTAINING CELLULAR ONCOGENE
    NIH/NCI R01CA065567Aug 15, 1995 - Apr 30, 2001
    Role: Principal Investigator

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    Publications listed below are automatically derived from MEDLINE/PubMed and other sources, which might result in incorrect or missing publications. Researchers can login to make corrections and additions, or contact us for help.
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    1. Zou M, Bhatia A, Dong H, Jayaprakash P, Guo J, Sahu D, Hou Y, Tsen F, Tong C, O'Brien K, Situ AJ, Schmidt T, Chen M, Ying Q, Ulmer TS, Woodley DT, Li W. Evolutionarily conserved dual lysine motif determines the non-chaperone function of secreted Hsp90alpha in tumour progression. Oncogene. 2017 04; 36(15):2160-2171. PMID: 27721406.
      View in: PubMed
    2. Bhatia A, O'Brien K, Chen M, Woodley DT, Li W. Keratinocyte-Secreted Heat Shock Protein-90alpha: Leading Wound Reepithelialization and Closure. Adv Wound Care (New Rochelle). 2016 Apr 01; 5(4):176-184. PMID: 27076995.
      View in: PubMed
    3. Dong H, Zou M, Bhatia A, Jayaprakash P, Hofman F, Ying Q, Chen M, Woodley DT, Li W. Breast Cancer MDA-MB-231 Cells Use Secreted Heat Shock Protein-90alpha (Hsp90a) to Survive a Hostile Hypoxic Environment. Sci Rep. 2016 Feb 05; 6:20605. PMID: 26846992.
      View in: PubMed
    4. Jayaprakash P, Dong H, Zou M, Bhatia A, O'Brien K, Chen M, Woodley DT, Li W. Hsp90a and Hsp90ß together operate a hypoxia and nutrient paucity stress-response mechanism during wound healing. J Cell Sci. 2015 Apr 15; 128(8):1475-80. PMID: 25736295.
      View in: PubMed
    5. O'Brien K, Bhatia A, Tsen F, Chen M, Wong AK, Woodley DT, Li W. Identification of the critical therapeutic entity in secreted Hsp90a that promotes wound healing in newly re-standardized healthy and diabetic pig models. PLoS One. 2014; 9(12):e113956. PMID: 25464502.
      View in: PubMed
    6. Tsen F, Bhatia A, O'Brien K, Cheng CF, Chen M, Hay N, Stiles B, Woodley DT, Li W. Extracellular heat shock protein 90 signals through subdomain II and the NPVY motif of LRP-1 receptor to Akt1 and Akt2: a circuit essential for promoting skin cell migration in vitro and wound healing in vivo. Mol Cell Biol. 2013 Dec; 33(24):4947-59. PMID: 24126057.
      View in: PubMed
    7. Li W, Tsen F, Sahu D, Bhatia A, Chen M, Multhoff G, Woodley DT. Extracellular Hsp90 (eHsp90) as the actual target in clinical trials: intentionally or unintentionally. Int Rev Cell Mol Biol. 2013; 303:203-35. PMID: 23445811.
      View in: PubMed
    8. Han A, Bandyopadhyay B, Jayaprakash P, Lua I, Sahu D, Chen M, Woodley DT, Li W. The anti-motility signaling mechanism of TGFß3 that controls cell traffic during skin wound healing. Biol Open. 2012 Dec 15; 1(12):1169-77. PMID: 23259050.
      View in: PubMed
    9. Sahu D, Zhao Z, Tsen F, Cheng CF, Park R, Situ AJ, Dai J, Eginli A, Shams S, Chen M, Ulmer TS, Conti P, Woodley DT, Li W. A potentially common peptide target in secreted heat shock protein-90a for hypoxia-inducible factor-1a-positive tumors. Mol Biol Cell. 2012 Feb; 23(4):602-13. PMID: 22190738.
      View in: PubMed
    10. Cheng CF, Sahu D, Tsen F, Zhao Z, Fan J, Kim R, Wang X, O'Brien K, Li Y, Kuang Y, Chen M, Woodley DT, Li W. A fragment of secreted Hsp90a 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. PMID: 22019588.
      View in: PubMed
    11. Li W, Sahu D, Tsen F. Secreted heat shock protein-90 (Hsp90) in wound healing and cancer. Biochim Biophys Acta. 2012 Mar; 1823(3):730-41. PMID: 21982864.
      View in: PubMed
    12. Bandyopadhyay B, Han A, Dai J, Fan J, Li Y, Chen M, Woodley DT, Li W. 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. PMID: 21172820.
      View in: PubMed
    13. Woodley DT, Fan J, Cheng CF, Li Y, Chen M, Bu G, Li W. 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. PMID: 19383717.
      View in: PubMed
    14. Woodley DT, Hou Y, Martin S, Li W, Chen M. Characterization of molecular mechanisms underlying mutations in dystrophic epidermolysis bullosa using site-directed mutagenesis. J Biol Chem. 2008 Jun 27; 283(26):17838-45. PMID: 18450758.
      View in: PubMed
    15. Cheng CF, Fan J, Fedesco M, Guan S, Li Y, Bandyopadhyay B, Bright AM, Yerushalmi D, Liang M, Chen M, Han YP, Woodley DT, Li W. 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. PMID: 18332123.
      View in: PubMed
    16. Li W, Li Y, Guan S, Fan J, Cheng CF, Bright AM, Chinn C, Chen M, Woodley DT. Extracellular heat shock protein-90alpha: linking hypoxia to skin cell motility and wound healing. EMBO J. 2007 Mar 07; 26(5):1221-33. PMID: 17304217.
      View in: PubMed
    17. Woodley DT, Remington J, Huang Y, Hou Y, Li W, Keene DR, Chen M. Intravenously injected human fibroblasts home to skin wounds, deliver type VII collagen, and promote wound healing. Mol Ther. 2007 Mar; 15(3):628-35. PMID: 17245357.
      View in: PubMed
    18. Bandyopadhyay B, Fan J, Guan S, Li Y, Chen M, Woodley DT, Li W. A "traffic control" role for TGFbeta3: orchestrating dermal and epidermal cell motility during wound healing. J Cell Biol. 2006 Mar 27; 172(7):1093-105. PMID: 16549496.
      View in: PubMed
    19. Woodley DT, Keene DR, Atha T, Huang Y, Lipman K, Li W, Chen M. Injection of recombinant human type VII collagen restores collagen function in dystrophic epidermolysis bullosa. Nat Med. 2004 Jul; 10(7):693-5. PMID: 15195089.
      View in: PubMed
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