Researcher Profile
Researcher Profile
Wei Li, PhD
Assistant Professor, Department of Pediatrics
Division of Hematology and Oncology
Assistant Professor, Department of Biochemistry and Molecular Biology
Division of Hematology and Oncology
Assistant 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
- Drosophila
Recent Publications
2020
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. https://doi.org/10.1073/pnas.2007598117
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. https://doi.org/10.15252/embr.202050642
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. https://doi.org/10.1038/s41467-020-19193-y
2019
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. https://doi.org/10.1242/jcs.225714
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. https://doi.org/10.1038/s41467-019-11884-5
2018
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. https://doi.org/10.1002/ajmg.a.38675
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. https://doi.org/10.1038/s41388-018-0425-7
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. https://doi.org/10.1038/s41388-018-0626-0