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Yuanyuan Xu
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China Medical University

Bio: Dr. Xu got the PhD degree on Occupational and Environmental Health in China Medical University and did Postdoctoral research in National Institute of Environmental Health Sciences (NIEHS), USA. Her research mainly focuses on mechanisms underlying chemical carcinogenesis. She has over 100 publications in peer-reviewed academic journals, such as Environ Health Perspect, Redox Biol and Free Radic Biol Med. Her research work won 7 awards for young scientist from the Society of Toxicology (SOT), USA and IUTOX. She is the principal investigator of four grants form National Science Foundation of China, and is selected as the Outstanding Young Scientist in in Liaoning Province. Dr. Xu has served as a board member and Secretary/Treasurer in Metals Specialty Section, SOT, USA, as well as a working group member and consultant expert member of IARC/WHO Monographs. She also serves in editorial board of Toxicol Appl Pharmacol and Regul Toxicol Pharmacol. In addition, she is the vise director of the Key Laboratory of Environmental Stress and Chronic Disease Control and Prevention, Ministry of Education, China.

 

Abstract: Arsenic is a well-known human carcinogen. Though oxidative stress has been considered as a key event in arsenic carcinogenesis, accumulating evidence suggests that reductive stress instead of oxidative stress occurs in response to chronic arsenic exposure at an environmentally relevant dose. In multiple arsenic-malignantly transformed cells, the intracellular levels of reactive oxygen species are significantly decreased, with reduced oxidative stress induced by other oxidants. In early-life arsenic-exposed mice, the increased ratio of GSH to GSSG in blood and expression of antioxidative genes in the target organ are found in pups. Consistently, the constitutive activation of nuclear factor erythroid 2- related factor 2 (Nrf2), a master regulator of antioxidative system, has been observed in both arsenic-transformed cells and arsenic pro-carcinogenic mouse model. This so-called non-canonical activation of Nrf2 is, at least in part, mediated by dysregulation of microRNAs and blockage of autophagic flux. As a transcription factor, Nrf2 regulates a panel of genes encoding cell metabolism, detoxifying and antioxidative enzymes, as well as HIF1α. The constitutive activation of Nrf2 leads to metabolic reprograming endowing cells with proliferative and cancer stem cell-like characteristics, resistance to death caused by other environment challenges, and changes in of chemical bioactivation. All these factors contribute to malignant transformation of cells.


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Date Time Local Time Room Forum Session Role Topic
2025-10-17 14:50-15:10 2025-10-17,14:50-15:10Room 2 - Guobin Hall 2 Workshop

Workshop 03: Heavy Metal Toxicity and Human Health-1

Speaker The role of transcription factor Nrf2 in arsenic-induced malignant transformation and its underling mechanism