Neutrophils, a key component of the innate immune system, play a complex and dual role in the tumor microenvironment (TME), influencing both pro- and anti-tumor outcomes. As the most abundant leukocytes in humans, neutrophils are equipped with mechanisms such as reactive oxygen species (ROS) generation, degranulation, phagocytosis, and the formation of neutrophil extracellular traps (NETs), enabling them to interact with adaptive immune cells and tumor cells. Recent research highlights their heterogeneity, with tumor-associated neutrophils (TANs) exhibiting both pro- and anti-tumor functions depending on their activation status and the TME. TANs can promote tumor growth by enhancing regulatory T cell activity, secreting factors that modify the TME, and facilitating metastasis through NETs. However, they also possess antitumor capabilities, such as inducing apoptosis in cancer cells, modulating immune responses, and participating in antibody-dependent cellular cytotoxicity (ADCC). Neutrophils can also act as antigen-presenting cells (APCs), transporting tumor antigens to lymph nodes and presenting them to T cells. Their role in crosstalk with the adaptive immune system is significant, as they can enhance T cell function and support anti-tumor immunity. Neutrophils' ability to modulate tumor-associated microbiota and their involvement in immunosuppressive pathways, such as PD-L1/PD-1 interactions, further complicate their role in cancer. Understanding neutrophil plasticity and their interactions with the TME is crucial for developing targeted therapies that harness innate immunity to improve cancer treatment outcomes.Neutrophils, a key component of the innate immune system, play a complex and dual role in the tumor microenvironment (TME), influencing both pro- and anti-tumor outcomes. As the most abundant leukocytes in humans, neutrophils are equipped with mechanisms such as reactive oxygen species (ROS) generation, degranulation, phagocytosis, and the formation of neutrophil extracellular traps (NETs), enabling them to interact with adaptive immune cells and tumor cells. Recent research highlights their heterogeneity, with tumor-associated neutrophils (TANs) exhibiting both pro- and anti-tumor functions depending on their activation status and the TME. TANs can promote tumor growth by enhancing regulatory T cell activity, secreting factors that modify the TME, and facilitating metastasis through NETs. However, they also possess antitumor capabilities, such as inducing apoptosis in cancer cells, modulating immune responses, and participating in antibody-dependent cellular cytotoxicity (ADCC). Neutrophils can also act as antigen-presenting cells (APCs), transporting tumor antigens to lymph nodes and presenting them to T cells. Their role in crosstalk with the adaptive immune system is significant, as they can enhance T cell function and support anti-tumor immunity. Neutrophils' ability to modulate tumor-associated microbiota and their involvement in immunosuppressive pathways, such as PD-L1/PD-1 interactions, further complicate their role in cancer. Understanding neutrophil plasticity and their interactions with the TME is crucial for developing targeted therapies that harness innate immunity to improve cancer treatment outcomes.