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.
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Keywords:
Apoptosis;
MicroRNA;
PTEN/Akt signaling pathway;
Pituitary adenoma
Document Type: Research Article
Affiliations:
Department of Neurosurgery and Pituitary Tumor Center, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China
Publication date:
11 February 2014
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Formerly: Oncology Research Incorporating Anti-Cancer Drug Design
Oncology Research Featuring Preclinical and Clincal Cancer Therapeutics publishes research of the highest quality that contributes to an understanding of cancer in areas of molecular biology, cell biology, biochemistry, biophysics, genetics, biology, endocrinology, and immunology, as well as studies on the mechanism of action of carcinogens and therapeutic agents, reports dealing with cancer prevention and epidemiology, and clinical trials delineating effective new therapeutic regimens.
From Volume 23, Oncology Research Featuring Preclinical and Clinical Cancer Therapeutics is Open Access under the terms of the Creative Commons CC BY-NC-ND license.