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

Ruiqing Long | Zendy; Zhuohui Liu | Zendy; Jinghui Li | Zendy; Hualin Yu | Zendy

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

Author(s) -

Ruiqing Long,

Zhuohui Liu,

Jinghui Li,

Hualin Yu

Publication year - 2019

Publication title -

aging

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 1.473

H-Index - 90

ISSN - 1945-4589

DOI - 10.18632/aging.102300

Subject(s) - pi3k/akt/mtor pathway , metastasis , protein kinase b , cancer research , epithelial–mesenchymal transition , cell growth , chemistry , pituitary tumors , pituitary adenoma , cell culture , cell migration , cell , adenoma , medicine , endocrinology , biology , signal transduction , cancer , biochemistry , genetics

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.

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