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lated in various types of tumor, the expression levels of miR199b5p in ES cells remain to be elucidated. The mechanism underlying ES via the miRNA pathway remains to be elucidated. The present study demonstrated that miR199b5p was an important regulator in ES cells and its expression was downregulated in ES originated A673/TC252 cells. The ES cell lines, A673 and TC252, were transfected with an miR199b5p mimic to overexpress the levels of this miRNA. This forced expression of miR199b5p suppressed the cell proliferation and invasion, arrested cell cycle progression, and promoted cell apoptosis. Furthermore, CCNL1 was identified by bioinformatic software as a potential target gene of miR199b5p. Following this, the present study identified CCNL1 as a direct target of miR199b5p in ES cells. Taken together, the present study established a functional link between ES, miR199b5p and CCNL1, and suggested that miR199b5p acts as a tumor suppressor and may be of diagnostic and therapeutic importance for human ES.