MicroRNAs (miRNAs) are important regulators that are involved in the development of different types of tumors. MicroRNA-200c (miR-200c) has been characterized as a tumor suppressor or oncogene in different cancers. However, the role of miR-200c in pituitary tumorigenesis remains unknown. We observed that miR-200c was overexpressed in pituitary adenoma cell lines. We transfected a miR-200c inhibitor into pituitary adenoma cells (MMQ cell line) to inhibit miR-200c expression and found that the percentage of apoptotic MMQ cells increased. Using bioinformatics analyses, we predicted that the tumor suppressor gene PTEN was targeted by miR-200c, and we confirmed the presence of a functional miR-200c binding site in the 3'-UTR of PTEN using luciferase reporter assays. We determined that the inhibition of miR-200c expression can upregulate PTEN expression and decrease the expression of phosphorylated Akt (p-Akt). Furthermore, the siRNA-mediated knockdown of PTEN abrogated the effect of inhibiting miR-200c expression. Taken together, these findings suggest that miR-200c regulates pituitary tumor formation through the PTEN/Akt signaling pathway. Therefore, we propose that the inhibition of miR-200c could have therapeutic potential in pituitary adenoma.