Miz-1 promotes the proliferation of esophageal cancer cells via suppression of p21 and release of p21-arrested cyclin D1.

Tumorigenesis results from various types of dysregulation of oncogenes and tumor suppressors that influence cellular proliferation, differentiation, apoptosis and senescence. The transcription factor Myc-interacting zinc finger protein 1 (Miz-1) can either activate or repress gene expression in concert with binding partners including the Myc oncoprotein in several types of tumors. Known target genes of these complexes encode the cyclin-dependent kinase inhibitors such as cdkn2b (p15) and cdknla (p21). In the present study, we showed that the silencing of Miz-1 expression, through shRNA in a lentiviral vector, influenced various biological processes in two types of esophageal carcinoma cell lines. Silencing of the expression of Miz-1 inhibited cell proliferation and promoted apoptosis in vitro. Loss of Miz-1 reduced the migration ability in esophageal carcinoma cells. High expression of p21 and downregulation of cyclin D1 accompanied the knockdown of Miz-1. Our data demonstrated that esophageal cancer has a cell cycle arrest pathway via Miz-1, p21 and cyclin D1.