Tumor development is initiated by an accumulation of genetic and epigenetic alterations, which promote tumor initiation, invasion and metastasis (1,2). During the development of human neoplasms, the hallmarks of cancer are acquired, including the sustainment of proliferative signaling, the evasion of growth suppressors, the resistance to cell death, the enabling of replicative immortality, the induction of angiogenesis, the activation of invasion and metastasis, genome instability and mutations, the tumor promotion of inflammation, the deregulation of cellular energetics and the avoidance of immune destruction. These hallmarks aid in our understanding of the diversity of neoplastic disease (3). With the continuous development of cancer research, our understanding of the molecular pathogenesis of cancer has been enhanced. Increasing efforts in cancer research have been focused on the study of oncogenes, tumor suppressors and signaling pathways. Since the development of a more in‑depth understanding of the molecular etiology of carcinogenesis, specific oncogenes have been identified and have led to the generation of ‘molecular‑targeted therapy’ (4). The development of a ‘pan‑cancer’ therapy may be possible by targeting an oncogene which is ubiquitously overexpressed in almost all types of cancer and has a regulatory role in the multistep processes of carcinogenesis (5).
A novel gene that has been identified is AEG‑1 [also known as Metadherin (MTDH) and Lysine‑rich CEACAM1 co‑isolated (LYRIC)], which has emerged as a potentially crucial mediator of malignant tumors, and a key converging point of a complex network of oncogenic signaling pathways (6,7). AEG‑1/MTDH presents as an ideal target for the development of the next generation of effective cancer therapeutics