The Full Form of TNF is Tumor necrosis factor.

Tumor necrosis factor (TNF) is a multifunctional cytokine that plays important roles in diverse cellular events such as cell survival, proliferation, differentiation, and death. As a pro-inflammatory cytokine, TNF is secreted by inflammatory cells, which may be involved in inflammation-associated carcinogenesis. TNF exerts its biological functions through activating distinct signaling pathways such as nuclear factor κB (NF-κB) and c-Jun N-terminal kinase (JNK). NF-κB is a major cell survival signal that is anti-apoptotic while sustained JNK activation contributes to cell death. The crosstalk between the NF-κB and JNK is involved in determining cellular outcomes in response to TNF. In regard to cancer, TNF is a double-dealer. On one hand, TNF could be an endogenous tumor promoter, because TNF stimulates cancer cells’ growth, proliferation, invasion and metastasis, and tumor angiogenesis. On the other hand, TNF could be a cancer killer. The property of TNF in inducing cancer cell death renders it a potential cancer therapeutic, although much work is needed to reduce its toxicity for systematic TNF administration. Recent studies have focused on sensitizing cancer cells to TNF-induced apoptosis through inhibiting survival signals such as NF-κB, by combined therapy. In this article we provide an overview of the roles of TNF-induced signaling pathways in cancer biology with specific emphasis on carcinogenesis and cancer therapy.

Tumor necrosis factor (TNF, also referred to as TNFα) was identified in the late1970s as a cytokine produced by immune cells having a capacity to suppress tumor cell proliferation and induce tumor regression [1, 2]. TNF is a protein consisting of 157 amino acids and is synthesized as a membrane-bound protein (pro-TNF) that is released by TNF-converting enzyme (TACE)-mediated cleavage. Since the TNF gene was cloned in 1984, extensive research has revealed a variety of roles for TNF under physiological conditions such as in body development and immunity, and in pathological responses such as inflammation, tumor growth, transplant rejection, rheumatoid arthritis, and septic shock [3]. On the cellular level TNF exerts its effects through its receptors to activate distinct signaling pathways that regulate cell survival, proliferation, or death. Accordingly, complicated roles for TNF in cancer have emerged. On the one hand, its anticancer property is mainly through inducing cancer cell death, a process that could be used for cancer therapy. On the other hand, TNF stimulates proliferation, survival, migration, and angiogenesis in most cancer cells that are resistant to TNF-induced cytotoxicity, resulting in tumor promotion. Thus, TNF is a double-edged sword that could be either pro- or anti-tumorigenic. In this review, we focus on the roles and mechanism of TNF in cancer biology with specific emphasis on carcinogenesis and cancer therapy.