Research Paper Advance Articles
Intracellular and extracellular S100A9 trigger epithelial-mesenchymal transition and promote the invasive phenotype of pituitary adenoma through activation of AKT1
- 1 Department of Neurosurgery, The Second Affiliated Hospital of Chongqing Medical University, Chongqing, China
- 2 Department of Neurosurgery, Guizhou Provincial People’s Hospital, Guiyang, Guizhou, China
- 3 Department of Anesthesiology, Guizhou Provincial People's Hospital, Guiyang, Guizhou, China
Received: June 6, 2020 Accepted: July 30, 2020 Published: November 17, 2020https://doi.org/10.18632/aging.104072
How to Cite
Copyright: © 2020 Huang et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Pituitary adenoma (PA) is mostly benign intracranial tumor, but it also displays invasive growth characteristics and provokes challenging clinical conditions. S100A9 protein enhances tumor progression. In this study, we firstly demonstrated that both intracellular and extracellular S100A9 promoted the expression of Vimentin and Intercellular cell adhesion molecule-1 (ICAM-1), coupled with reduced E-cadherin in PA. As a result, PA acquired the phenotype of Epithelial-Mesenchymal Transition (EMT), leading to proliferation, cell cycle progression, migration and invasion. In addition, we indicated S100A9-induced EMT was mediated by activation of AKT1. Furthermore, immunohistochemistry showed that S100A9 expression was higher in invasive PA than that in non-invasive PA. These data extended our understanding for the effects of S100A9 on PA invasion and contributed to further development of a promising therapeutic target for invasive PA.