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
((Long R, Liu Z, Li J, Yu H. COL6A6 interacted with P4HA3 to suppress the growth
and metastasis of pituitary adenoma via blocking PI3K-Akt pathway. Aging (Albany 
NY). 2019 Oct 17;11. doi: 10.18632/aging.102300. [Epub ahead of print] PubMed
PMID: 31627190.
)).