Abstract: Tumor-associated neutrophils (TAN) are key components of the tumor microenvironment (TME) that exert dual regulatory roles in tumor progression through highly heterogeneous functional phenotypes. This review systematically addresses the dynamic balance of TAN in pro-tumor and anti-tumor mechanisms: TAN can directly kill tumor cells or collaborate with immune cells to activate anti-tumor responses; however, in contrast, they can accelerate tumor progression by promoting angiogenesis, remodeling the extracellular matrix, and mediating immune evasion. Studies have shown that the functional heterogeneity of TAN is precisely regulated by multiple signaling networks within the TME, and that the plasticity transformation of different subsets directly influences tumor progression. In-depth analyses of TAN subset characteristics, transformation mechanisms, and their clinical relevance will provide a theoretical basis for the development of inhibitors targeting pro-tumor neutrophils as well as advance the establishment of precise patient selection strategies for TAN subtype-based immunotherapy.