Tumor Necrosis Factor-α, a Regulator and Therapeutic Agent on Breast Cancer

The cell-mediated immunity and cytotoxic agents play a significant role on tumor cell apoptosis. Tumor necrosis factor-a (TNF-alpha) is an intricate linker between inflammation and cancer through mediating the process of apoptosis and cell-mediated immunity. A variety of evidences have confirmed the critical role of TNF-alpha on tumor migration, proliferation, matrix degradation, tumor metastasis, invasion, and angiogenesis. Through binding to receptors, TNF-alpha participates in activating multiple cell signaling cascades that link inflammation, survival and evolution towards breast cancer. TNF-alpha is an important agent for tumor biotherapy, but its clinical application is limited for its severe fatal systemic toxicity. The poly-lactic acid microspheres (PLAM) with intratumoral cytokine release hold tremendous potential for the immunotherapy of breast cancer, and TNF-alpha antagonists may offer therapeutic potential in solid tumors. In addition, TNF-alpha is related with the blockage of estrogen and progesterone receptors. For breast cancer treatment, it is necessary to understand the molecular signaling pathways that mediate TNF-alpha and the aggressive behavior of negative breast cancer. The aim of present review is to summarize the effect of TNF-alpha on breast cancer cells.