Apoptosis and epithelial-to-mesenchymal transition (EMT) are very fundamental physiological processes. They are both independent and interrelated events in normal development and in maintaining body homeostasis. In recent years, EMT has emerged as a focus of studies in cancer research, and increasing data indicate that EMT functions as a central step in the invasion and metastasis of some tumor cells. Besides the cytoskeleton rearrangement and subsequent morphological changes, EMT is often characterized by the dissolution or attenuation of epithelial adhesion and other polarized structures, for example, tight junctions, and by accordingly the acquisition of migratory and invasive properties of the cells undergoing EMT. Along with these changes, EMT can be associated with transcriptional or expressional alterations of some epithelial and mesenchymal genes.

Dysregulation of apoptosis and EMT are linked with various pathological processes, such as fibrosis of liver and kidney, vascular diseases, abnormal development of embryos, tumor formation and progression [1-5]. Transforming growth factor-β (TGF-β) is a potent pleiotropic molecule that is implicated in diverse biological processes. Interestingly, TGF-β is involved in the tight control of both apoptosis and EMT, which are key to TGF-β’s role in physiological and pathological events. Thus, exploring the mechanisms of apoptosis and EMT and their regulation by TGF-β can be of great importance in seeking new therapeutic targets for tumor and other diseases. TGF-β1 treatment induced strong apoptosis of mouse hepatocytes (AML-12) in dose-and time-dependent manners. The apoptotic response of cells was only apparent after 24 h and lasted for several days, until the death of