Wei Li, PhD

Title(s)Professor of Dermatology
SchoolKeck School of Medicine of Usc
AddressNOR 5301 1441 Eastlake Avenue
Health Sciences Campus
Los Angeles CA 90089-9176
Phone+1 323 865 0618
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    Other Positions
    Title(s)Director, MSS Graduate Program


    Collapse Biography 
    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 R01AR059853Jul 1, 2011 - Apr 30, 2018
    Role: Principal Investigator
    Mechanisms of Human Dermal Fibroblast Migration
    NIH R01GM067100Jan 1, 2003 - Apr 30, 2021
    Role: Principal Investigator
    Signal Transduction of Human Keratinocyte Migration
    NIH R01GM066193Jul 1, 2002 - May 31, 2013
    Role: Principal Investigator
    STUDIES OF A NOVEL SH2/SH3-CONTAINING CELLULAR ONCOGENE
    NIH R01CA065567Aug 15, 1995 - Apr 30, 2001
    Role: Principal Investigator

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      Collapse Publications
      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. to make corrections and additions.
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      Altmetrics Details PMC Citations indicate the number of times the publication was cited by articles in PubMed Central, and the Altmetric score represents citations in news articles and social media. (Note that publications are often cited in additional ways that are not shown here.) Fields are based on how the National Library of Medicine (NLM) classifies the publication's journal and might not represent the specific topic of the publication. Translation tags are based on the publication type and the MeSH terms NLM assigns to the publication. Some publications (especially newer ones and publications not in PubMed) might not yet be assigned Field or Translation tags.) Click a Field or Translation tag to filter the publications.
      1. Evolutionarily conserved dual lysine motif determines the non-chaperone function of secreted Hsp90alpha in tumour progression. Oncogene. 2017 04; 36(15):2160-2171. 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. PMID: 27721406; PMCID: PMC5386837.
        View in: PubMed   Mentions: 25     Fields:    Translation:HumansCells
      2. Keratinocyte-Secreted Heat Shock Protein-90alpha: Leading Wound Reepithelialization and Closure. Adv Wound Care (New Rochelle). 2016 Apr 01; 5(4):176-184. Bhatia A, O'Brien K, Chen M, Woodley DT, Li W. PMID: 27076995; PMCID: PMC4817596.
        View in: PubMed   Mentions: 11     Fields:    
      3. Breast Cancer MDA-MB-231 Cells Use Secreted Heat Shock Protein-90alpha (Hsp90α) to Survive a Hostile Hypoxic Environment. Sci Rep. 2016 Feb 05; 6:20605. Dong H, Zou M, Bhatia A, Jayaprakash P, Hofman F, Ying Q, Chen M, Woodley DT, Li W. PMID: 26846992; PMCID: PMC4742873.
        View in: PubMed   Mentions: 28     Fields:    Translation:HumansCells
      4. Hsp90α and Hsp90β together operate a hypoxia and nutrient paucity stress-response mechanism during wound healing. J Cell Sci. 2015 Apr 15; 128(8):1475-80. Jayaprakash P, Dong H, Zou M, Bhatia A, O'Brien K, Chen M, Woodley DT, Li W. PMID: 25736295; PMCID: PMC4518443.
        View in: PubMed   Mentions: 29     Fields:    Translation:HumansAnimalsCells
      5. Identification of the critical therapeutic entity in secreted Hsp90α that promotes wound healing in newly re-standardized healthy and diabetic pig models. PLoS One. 2014; 9(12):e113956. O'Brien K, Bhatia A, Tsen F, Chen M, Wong AK, Woodley DT, Li W. PMID: 25464502; PMCID: PMC4252061.
        View in: PubMed   Mentions: 11     Fields:    Translation:Animals
      6. 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. Tsen F, Bhatia A, O'Brien K, Cheng CF, Chen M, Hay N, Stiles B, Woodley DT, Li W. PMID: 24126057; PMCID: PMC3889557.
        View in: PubMed   Mentions: 39     Fields:    Translation:AnimalsCells
      7. Extracellular Hsp90 (eHsp90) as the actual target in clinical trials: intentionally or unintentionally. Int Rev Cell Mol Biol. 2013; 303:203-35. Li W, Tsen F, Sahu D, Bhatia A, Chen M, Multhoff G, Woodley DT. PMID: 23445811; PMCID: PMC4023563.
        View in: PubMed   Mentions: 36     Fields:    Translation:HumansCells
      8. The anti-motility signaling mechanism of TGFβ3 that controls cell traffic during skin wound healing. Biol Open. 2012 Dec 15; 1(12):1169-77. Han A, Bandyopadhyay B, Jayaprakash P, Lua I, Sahu D, Chen M, Woodley DT, Li W. PMID: 23259050; PMCID: PMC3522877.
        View in: PubMed   Mentions: 8     Fields:    
      9. 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. 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. PMID: 22190738; PMCID: PMC3279389.
        View in: PubMed   Mentions: 33     Fields:    Translation:HumansAnimalsCells
      10. 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. 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. PMID: 22019588; PMCID: PMC3204835.
        View in: PubMed   Mentions: 54     Fields:    Translation:HumansAnimalsCells
      11. Secreted heat shock protein-90 (Hsp90) in wound healing and cancer. Biochim Biophys Acta. 2012 Mar; 1823(3):730-41. Li W, Sahu D, Tsen F. PMID: 21982864; PMCID: PMC3266443.
        View in: PubMed   Mentions: 75     Fields:    Translation:HumansAnimalsCells
      12. 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. Bandyopadhyay B, Han A, Dai J, Fan J, Li Y, Chen M, Woodley DT, Li W. PMID: 21172820; PMCID: PMC3001406.
        View in: PubMed   Mentions: 19     Fields:    Translation:HumansCells
      13. 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. Woodley DT, Fan J, Cheng CF, Li Y, Chen M, Bu G, Li W. PMID: 19383717; PMCID: PMC2680098.
        View in: PubMed   Mentions: 31     Fields:    Translation:HumansCells
      14. Characterization of molecular mechanisms underlying mutations in dystrophic epidermolysis bullosa using site-directed mutagenesis. J Biol Chem. 2008 Jun 27; 283(26):17838-45. Woodley DT, Hou Y, Martin S, Li W, Chen M. PMID: 18450758; PMCID: PMC2440610.
        View in: PubMed   Mentions: 12     Fields:    Translation:HumansCells
      15. 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. 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. PMID: 18332123; PMCID: PMC2423165.
        View in: PubMed   Mentions: 103     Fields:    Translation:HumansCells
      16. Extracellular heat shock protein-90alpha: linking hypoxia to skin cell motility and wound healing. EMBO J. 2007 Mar 07; 26(5):1221-33. Li W, Li Y, Guan S, Fan J, Cheng CF, Bright AM, Chinn C, Chen M, Woodley DT. PMID: 17304217; PMCID: PMC1817627.
        View in: PubMed   Mentions: 130     Fields:    Translation:HumansAnimalsCells
      17. Intravenously injected human fibroblasts home to skin wounds, deliver type VII collagen, and promote wound healing. Mol Ther. 2007 Mar; 15(3):628-35. Woodley DT, Remington J, Huang Y, Hou Y, Li W, Keene DR, Chen M. PMID: 17245357.
        View in: PubMed   Mentions: 40     Fields:    Translation:HumansAnimalsCells
      18. 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. Bandyopadhyay B, Fan J, Guan S, Li Y, Chen M, Woodley DT, Li W. PMID: 16549496; PMCID: PMC2063766.
        View in: PubMed   Mentions: 59     Fields:    Translation:HumansCells
      19. Injection of recombinant human type VII collagen restores collagen function in dystrophic epidermolysis bullosa. Nat Med. 2004 Jul; 10(7):693-5. Woodley DT, Keene DR, Atha T, Huang Y, Lipman K, Li W, Chen M. PMID: 15195089.
        View in: PubMed   Mentions: 43     Fields:    Translation:HumansAnimals
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      NIH Funding Acknowledgment: Important - All publications resulting from the utilization of SC CTSI resources are required to credit the SC CTSI grant by including the NIH funding acknowledgment and must comply with the NIH Public Access Policy.

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