Researcher Profile

Researcher Profile

Wei Li, PhD

Wei Li, PhD

Associate Professor, Department of Pediatrics
Division of Hematology and Oncology
Associate Professor, Department of Biochemistry and Molecular Biology
Scientific Program:Mechanisms of Carcinogenesis

Research Interests

Dr. Wei Li’s laboratory is interested in studying intercellular interactions during tissue homeostasis and determining how de-regulated interactions among cells promote cell transformation and tumor progression. His research integrates molecular, cellular and biochemical approaches in combination with mouse tumorigenesis models. Currently, Dr. Li’s laboratory focuses on elucidating the regulation and function of the Hippo tumor suppressor pathway in brain tumors. The goal of Dr. Li’s research is to find molecular targets and biomarkers for cancer therapy.

  • Neoplasms
  • Neurofibromin 2
  • Carcinogenesis
  • Ubiquitin-Protein Ligases
  • Genes
  • Growth
  • Glioblastoma
  • Mutation
  • Neurofibromatosis 2
  • Proteins
  • Glioma
  • Necrosis

Recent Publications


Yee, PP & Li, W 2021, 'Tumor necrosis: A synergistic consequence of metabolic stress and inflammation', BioEssays, vol. 43, no. 7, 2100029.


Johnson, MT, Gudlur, A, Zhang, X, Xin, P, Emrich, SM, Yoast, RE, Courjaret, R, Nwokonko, RM, Li, W, Hempel, N, Machaca, K, Gill, DL, Hogan, PG & Trebak, M 2020, 'L-type Ca2+ channel blockers promote vascular remodeling through activation of STIM proteins', Proceedings of the National Academy of Sciences of the United States of America, vol. 117, no. 29, pp. 17369-17380.
Wei, Y, Yee, PP, Liu, Z, Zhang, L, Guo, H, Zheng, H, Anderson, B, Gulley, M & Li, W 2020, 'NEDD4L-mediated Merlin ubiquitination facilitates Hippo pathway activation', EMBO Reports, vol. 21, no. 12, e50642.
Yee, PP, Wei, Y, Kim, SY, Lu, T, Chih, SY, Lawson, C, Tang, M, Liu, Z, Anderson, B, Thamburaj, K, Young, MM, Aregawi, DG, Glantz, MJ, Zacharia, BE, Specht, CS, Wang, HG & Li, W 2020, 'Neutrophil-induced ferroptosis promotes tumor necrosis in glioblastoma progression', Nature communications, vol. 11, no. 1, 5424.


Liu, Z, Yee, PP, Wei, Y, Liu, Z, Imamura, Y & Li, W 2019, 'Differential YAP expression in glioma cells induces cell competition and promotes tumorigenesis', Journal of Cell Science, vol. 132, no. 5, jcs225714.
Pajtler, KW, Wei, Y, Okonechnikov, K, Silva, PBG, Vouri, M, Zhang, L, Brabetz, S, Sieber, L, Gulley, M, Mauermann, M, Wedig, T, Mack, N, Imamura Kawasawa, Y, Sharma, T, Zuckermann, M, Andreiuolo, F, Holland, E, Maass, K, Körkel-Qu, H, Liu, HK, Sahm, F, Capper, D, Bunt, J, Richards, LJ, Jones, DTW, Korshunov, A, Chavez, L, Lichter, P, Hoshino, M, Pfister, SM, Kool, M, Li, W & Kawauchi, D 2019, 'YAP1 subgroup supratentorial ependymoma requires TEAD and nuclear factor I-mediated transcriptional programmes for tumorigenesis', Nature communications, vol. 10, no. 1, 3914.


Fisher, MJ, Belzberg, AJ, de Blank, P, De Raedt, T, Elefteriou, F, Ferner, RE, Giovannini, M, Harris, GJ, Kalamarides, M, Karajannis, MA, Kim, AR, Lázaro, C, Le, LQ, Li, W, Listernick, R, Martin, S, Morrison, H, Pasmant, E, Ratner, N, Schorry, E, Ullrich, NJ, Viskochil, D, Weiss, B, Widemann, BC, Zhu, Y, Bakker, A & Serra, E 2018, '2016 Children's Tumor Foundation conference on neurofibromatosis type 1, neurofibromatosis type 2, and schwannomatosis', American Journal of Medical Genetics, Part A, vol. 176, no. 5, pp. 1258-1269.
Liu, Z, Wei, Y, Zhang, L, Yee, PP, Johnson, M, Zhang, X, Gulley, M, Atkinson, JM, Trebak, M, Wang, H-G & Li, W 2019, 'Induction of store-operated calcium entry (SOCE) suppresses glioblastoma growth by inhibiting the Hippo pathway transcriptional coactivators YAP/TAZ', Oncogene, vol. 38, no. 1, pp. 120-139.
Zhang, L, Cheng, F, Wei, Y, Zhang, L, Guo, D, Wang, B & Li, W 2019, 'Inhibition of TAZ contributes radiation-induced senescence and growth arrest in glioma cells', Oncogene, vol. 38, no. 15, pp. 2788-2799.

Clinical Trials Search

Children (age < 18 years)
Adults (age >= 18 years)