RNA-binding proteins (RBPs) play essential roles in RNA metabolism, regulating RNA splicing, transport, surveillance, decay and translation. The aberrant expression of RBPs leads to gene expression alteration and frequently causes various diseases, such as cancer. In this study, we are the first to provide evidence that hMex-3A, a RBP that belongs to the human Mex-3 family with two K-homology RNA-binding domains, is involved in the regulation of tumorigenesis. We show that the silencing of hMex-3A by small interference RNA effectively inhibits cell proliferation in SNU-16 and AGS gastric cancer cells. Flow cytometry analysis confirmed this effect on SNU-16 cell growth and indicated that hMex-3A may function in the G1/M phase. Notably, hMex-3A knockdown also reduced the colony formation ability of SNU-16 and AGS cells in soft agar, implying that hMex-3A is required for cell transformation. Furthermore, the hMex-3A knockdown markedly affected the migratory ability of BCG-823 cells by transwell chamber and wound healing assays. Clinical relevance analysis using 22 paired gastric cancer specimens by quantitative real-time PCR showed that hMex-3A was significantly upregulated (63.6%) in cancer tissues compared with matched adjacent non-cancerous tissues. Taken together, these results suggest that hMex-3A functions as an oncogene candidate in the development and metastasis of gastric cancer; thus it may serve as a potential target for the therapy of tumors.