The transcription factor NF-κB is a key regulator of genes involved in immune and inflammatory responses, and its activation has been linked to various aspects of oncogenesis, including apoptosis, cell cycle control, differentiation, and cell migration. Dysregulation of NF-κB is common in many cancers, and its inhibition is a promising therapeutic strategy. NF-κB is regulated by the IκB proteins, which inhibit its nuclear translocation. Upon stimulation, IκB proteins are phosphorylated and degraded, allowing NF-κB to enter the nucleus and activate gene expression. NF-κB is involved in oncogenesis through its role in promoting cell survival, proliferation, and resistance to apoptosis, as well as in facilitating metastasis and angiogenesis. It can also be activated by viral oncoproteins and oncogenic signals, contributing to transformation. NF-κB's antiapoptotic and pro-proliferative functions are crucial in cancer progression, but it can also play a proapoptotic role in certain contexts. Inhibiting NF-κB has shown promise in cancer therapy, as it can enhance the effectiveness of chemotherapeutic agents and radiation by increasing apoptosis. However, the complex roles of NF-κB in different cancers and its interactions with other pathways, such as p53, require further investigation. Inhibiting NF-κB is a potential adjuvant therapy in cancer treatment, particularly in cancers where NF-κB is constitutively active. The inhibition of NF-κB can be achieved through various means, including the use of small molecule inhibitors and genetic approaches, and it has shown potential in preclinical studies for improving chemotherapeutic responses. Despite its therapeutic potential, challenges remain in targeting NF-κB effectively in different cancer types.The transcription factor NF-κB is a key regulator of genes involved in immune and inflammatory responses, and its activation has been linked to various aspects of oncogenesis, including apoptosis, cell cycle control, differentiation, and cell migration. Dysregulation of NF-κB is common in many cancers, and its inhibition is a promising therapeutic strategy. NF-κB is regulated by the IκB proteins, which inhibit its nuclear translocation. Upon stimulation, IκB proteins are phosphorylated and degraded, allowing NF-κB to enter the nucleus and activate gene expression. NF-κB is involved in oncogenesis through its role in promoting cell survival, proliferation, and resistance to apoptosis, as well as in facilitating metastasis and angiogenesis. It can also be activated by viral oncoproteins and oncogenic signals, contributing to transformation. NF-κB's antiapoptotic and pro-proliferative functions are crucial in cancer progression, but it can also play a proapoptotic role in certain contexts. Inhibiting NF-κB has shown promise in cancer therapy, as it can enhance the effectiveness of chemotherapeutic agents and radiation by increasing apoptosis. However, the complex roles of NF-κB in different cancers and its interactions with other pathways, such as p53, require further investigation. Inhibiting NF-κB is a potential adjuvant therapy in cancer treatment, particularly in cancers where NF-κB is constitutively active. The inhibition of NF-κB can be achieved through various means, including the use of small molecule inhibitors and genetic approaches, and it has shown potential in preclinical studies for improving chemotherapeutic responses. Despite its therapeutic potential, challenges remain in targeting NF-κB effectively in different cancer types.