From inflammation to invasion: neutrophils in cervical cancer pathogenesis

Cervical cancer, predominantly caused by high-risk human papillomavirus (HPV) infections, continues to be a major health challenge globally. Recent research has highlighted the significant role of neutrophils, a type of white blood cell integral to the immune system, in the pathogenesis of cervical cancer. This review examines the dualistic role of neutrophils in cervical cancer, emphasizing their contribution to both inflammation and tumor progression. Understanding the intricate relationship between neutrophils and cervical cancer could unveil new therapeutic targets for better disease management. Neutrophils are key mediators of the immune response and inflammation. In the context of cervical cancer, these cells are recruited to the tumor microenvironment where they can adopt tumor-promoting phenotypes. Tumor-associated neutrophils (TANs) facilitate various processes that aid tumor growth and metastasis, such as producing reactive oxygen species (ROS) and proteases that induce DNA damage, releasing cytokines and chemokines that promote angiogenesis, and forming neutrophil extracellular traps (NETs) that enhance metastatic potential. Furthermore, TANs contribute to immune suppression by inhibiting the activity of cytotoxic T lymphocytes and natural killer cells, allowing cancer cells to evade immune surveillance. Given their pivotal role in cervical cancer progression, neutrophils represent a promising target for novel therapeutic strategies. Approaches such as inhibiting neutrophil recruitment to the tumor site, blocking NET formation, and modulating TAN phenotypes from pro-tumor to anti-tumor are being explored. These strategies aim to disrupt the supportive role of neutrophils in tumor development and progression, potentially leading to improved outcomes for patients with cervical cancer.