Decoding the Molecular Mechanisms of BRAFV600E-Induced Nevi Formation  

作　　者：Weizheng Liang Yuxuan Liu Dandan Xu Wenjie Jiang Rensen Ran 

机构地区：[1]Central Laboratory,The First Affiliated Hospital of Hebei North University,Zhangjiakou 075000,Hebei,China [2]Institute of Molecular Immunology,School of Laboratory Medicine and Biotechnology,Southern Medical University,Guangzhou 510515,Guangdong,China [3]Department of Artificial Intelligence and Data Science,Hebei University of Technology,Tianjin 300401,China [4]Department of Chemical Biology,School of Life Sciences,Southern University of Science and Technology,Shenzhen 518055,Guangdong,China

出　　处：《Biomedical and Environmental Sciences》2024年第7期774-784,共11页生物医学与环境科学（英文版）

摘　　要：Melanocytes derived from neural crest cells harbor the BRAFV600E mutation,which is the predominant driver of nevus formation in humans.This mutation leads to malignant cell proliferation and subsequent cell cycle arrest,culminating in oncogene-induced senescence and nevus development.Nevertheless,emerging evidence has highlighted the heterogeneity of cellular senescence markers in BRAFV600E-induced senescent melanocytes.Moreover,the capacity of melanocytes within nevi to regain their proliferative ability raises questions about the molecular mechanisms by which BRAFV600E,via the mitogen-activated protein kinase signaling pathway,triggers nevus formation.This study provides an overview and discussion of the molecular mechanisms underpinning BRAFV600E-induced melanocyte nevus formation and the relevant animal models employed for their elucidation.It also highlights the significance of elucidating dynamic changes in cytoplasmic and nuclear substrates that interact with phosphorylated extracellular signal-regulated protein kinases 1 and 2 and underscores the value of using targeted BRAFV600E animal models created through gene editing technologies.

关 键 词：BRAFV600E MELANOCYTES NEVI Oncogene-induced senescence Animal models 

分 类 号：R758.51[医药卫生—皮肤病学与性病学]