Lei Wang
- Assistant Research Professor
- Member of the Graduate Faculty
Contact
- (520) 626-2823
- Pharmacy, Rm. 345
- Tucson, AZ 85721
- leiw1@arizona.edu
Biography
Lei WangAssistant Research Professor
leiw1@arizona.edu
Dr. Wang is an Assistant Research Professor in the Department of Pharmacology and Toxicology, College of Pharmacy, University of Arizona. He works in the field of cancer biology, molecular biology, toxicology, pharmacology and drug discovery. He is interested in RNA binding proteins under physiological and pathological conditions.
Areas of Research:
RNA binding proteins and RNA metabolism
RNA binding proteins in cancer
Environmental factor related carcinogenesis
Degree(s)
PhD, East China Normal University, Shanghai, China, 2007
M.S., Yunnan Agricultural University, Kunming, China, 2004
B.S., Henan Normal University, Henan Normal University, Xinxiang, China, 1997
Degrees
- Ph.D.
Interests
Teaching
BiochemistryCancer biology
Research
Areas of Research:RNA binding proteins and RNA metabolismRNA binding proteins in cancerEnvironmental factor related carcinogenesis
Courses
No activities entered.
Scholarly Contributions
Journals/Publications
- Shaw, B., Thwin, P. H., Jia, N., Weng, H., Ma, C., Zhu, H., & Wang, L. (2024). Stress granules play a critical role in hexavalent chromium-induced malignancy in a G3BP1 dependent manner. Environmental pollution (Barking, Essex : 1987), 362, 124997.More infoStress granules (SGs) are dynamic membraneless organelles influencing multiple cellular pathways including cell survival, proliferation, and malignancy. Hexavalent chromium [Cr(VI)] is a toxic heavy metal associated with severe environmental health risks. Low-level environmental exposure to Cr(VI) has been reported to cause cancer, but the role of SGs in Cr(VI)-induced health effects remains unclear. This study was intended to elucidate the impact of Cr(VI) exposure on SG dynamics and the role of SGs in Cr(VI)-induced malignancy. Results showed that both acute exposure to high concentration of Cr(VI) and prolonged exposure to low concentration of Cr(VI)-induced SG formation in human bronchial epithelium BEAS-2B cells. Cells pre-exposed to Cr(VI) exhibited a more robust SG response compared to cells without pre-exposure. An up-regulated SG response was associated with increased malignant properties in cells exposed to low concentration Cr(VI) for an extended period of time up to 12 months. Knocking out the SG core protein G3BP1 in Cr(VI)-transformed (CrT) cells reduced SG formation and malignant properties, including proliferation rate, sphere formation, and malignant markers. The results support a critical role for SGs in mediating Cr(VI)-induced malignancy in a G3BP1-dependent manner, representing a novel mechanism and a potential therapeutic target.
