POU5F1 and neoplasm: However, although the expression of AKT1 was also sharply reduced and cell proliferation was accelerated by miR-302 upregulation in hMSCs, overexpression of miR-302 did not lead OCT4 negative hMSCs to acquire the ability of tumor formation, which suggested that the regulation of miR-302 on pluripotency and teratoma formation may be dependent on the high endogenous expression of OCT4 in cells.