Intestinal epithelium undergoes a continuous self-renewal to maintain the intestinal homeostasis. Recently, we identified ZIP7 as a novel zinc transporter, securing of vigorous proliferation of immature intestinal epithelial cells that are called transit-amplifying (TA) cells by resolving endoplasmic reticulum (ER) stress. Dysregulation of cell proliferation machinery has been implicated in tumorigenesis. In this study, we investigated the role of ZIP7 in colorectal cancer development. siRNA or shRNA knockdown of ZIP7 suppressed cell proliferation, which was assessed by cell counting assay or crystal violet analysis, in human colorectal cancer cell lines. Apoptotic cell death was caused by siRNA knockdown of ZIP7, suggesting that ZIP7 is required for survival of colon cancer cells. Xenograft assays in immunodeficient mice showed that tumors generated by ZIP7-depleted cells were smaller than those generated by control cells, showing the requirement of ZIP7 expression in cancer cells for tumorigenicity in vivo. Furthermore, we found that overexpression of ZIP7 substantially increased volumes and weights of the xenograft tumors. These findings suggest that ZIP7 not only is required for tumor formation but also promotes tumorigenesis and thus, represents an attractive therapeutic target for colorectal cancer.