Research Paper|Volume 11, Issue 20|pp 8845—8859

COL6A6 interacted with P4HA3 to suppress the growth and metastasis of pituitary adenoma via blocking PI3K-Akt pathway

Ruiqing Long¹, Zhuohui Liu², Jinghui Li¹, Hualin Yu¹

¹Department of Neurosurgery, The First Affiliated Hospital of Kunming Medical University, Kunming 650032, Yunnan, China
²Department of Otolaryngology, The First Affiliated Hospital of Kunming Medical University, Kunming 650032, Yunnan, China

Received: June 14, 2019Accepted: September 15, 2019Published: October 17, 2019

Copyright © 2019 Long 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.

Abstract

The role and mechanism of collagen type VI alpha 6 (COL6A6) on tumor growth and metastasis in pituitary adenoma (PA) was determined. COL6A6 was downregulated in PA tissues and cell lines, which was negatively associated with the expression of prolyl-4-hydroxylase alpha polypeptide III (P4HA3) in the progression of PA. Overexpression of COL6A6 significantly suppressed tumor growth and metastasis capacity in PA. In addition, P4HA3 worked as the upstream of the PI3K-Akt pathway to alleviate the antitumor activity of COL6A6 on the growth and metastasis of both AtT-20 and HP75 cells. Furthermore, the inhibitory effect of COL6A6 on cell proliferation, migration and invasion, and epithelial-mesenchymal transition (EMT) was reversed by P4HA3 overexpression or activation of the PI3K-Akt pathway induced by IGF-1 addition, which provided a new biomarker for clinical PA treatment.