COL6A6 interacted with P4HA3 to suppress the growth and metastasis of pituitary adenoma via blocking PI3K-Akt pathway
Identifieur interne : 000981 ( Main/Exploration ); précédent : 000980; suivant : 000982COL6A6 interacted with P4HA3 to suppress the growth and metastasis of pituitary adenoma via blocking PI3K-Akt pathway
Auteurs : Ruiqing Long [République populaire de Chine] ; Zhuohui Liu [République populaire de Chine] ; Jinghui Li [République populaire de Chine] ; Hualin Yu [République populaire de Chine]Source :
- Aging (Albany NY) [ 1945-4589 ] ; 2019.
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.
Url:
DOI: 10.18632/aging.102300
PubMed: 31627190
PubMed Central: 6834431
Affiliations:
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China</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Neurosurgery, The First Affiliated Hospital of Kunming Medical University, Kunming 650032, Yunnan</wicri:regionArea><wicri:noRegion>Yunnan</wicri:noRegion></affiliation></author><author><name sortKey="Liu, Zhuohui" sort="Liu, Zhuohui" uniqKey="Liu Z" first="Zhuohui" last="Liu">Zhuohui Liu</name><affiliation wicri:level="1"><nlm:aff id="aff2">Department of Otolaryngology, The First Affiliated Hospital of Kunming Medical University, Kunming 650032, Yunnan, China</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Otolaryngology, The First Affiliated Hospital of Kunming Medical University, Kunming 650032, Yunnan</wicri:regionArea><wicri:noRegion>Yunnan</wicri:noRegion></affiliation></author><author><name sortKey="Li, Jinghui" sort="Li, Jinghui" uniqKey="Li J" first="Jinghui" last="Li">Jinghui Li</name><affiliation wicri:level="1"><nlm:aff id="aff1">Department of Neurosurgery, The First Affiliated Hospital of Kunming Medical University, Kunming 650032, Yunnan, China</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Neurosurgery, The First Affiliated Hospital of Kunming Medical University, Kunming 650032, Yunnan</wicri:regionArea><wicri:noRegion>Yunnan</wicri:noRegion></affiliation></author><author><name sortKey="Yu, Hualin" sort="Yu, Hualin" uniqKey="Yu H" first="Hualin" last="Yu">Hualin Yu</name><affiliation wicri:level="1"><nlm:aff id="aff1">Department of Neurosurgery, The First Affiliated Hospital of Kunming Medical University, Kunming 650032, Yunnan, China</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Neurosurgery, The First Affiliated Hospital of Kunming Medical University, Kunming 650032, Yunnan</wicri:regionArea><wicri:noRegion>Yunnan</wicri:noRegion></affiliation></author></analytic><series><title level="j">Aging (Albany NY)</title><idno type="eISSN">1945-4589</idno><imprint><date when="2019">2019</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>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.</p></div></front><back><div1 type="bibliography"><listBibl><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct></listBibl></div1></back></TEI><affiliations><list><country><li>République populaire de Chine</li></country></list><tree><country name="République populaire de Chine"><noRegion><name sortKey="Long, Ruiqing" sort="Long, Ruiqing" uniqKey="Long R" first="Ruiqing" last="Long">Ruiqing Long</name></noRegion><name sortKey="Li, Jinghui" sort="Li, Jinghui" uniqKey="Li J" first="Jinghui" last="Li">Jinghui Li</name><name sortKey="Liu, Zhuohui" sort="Liu, Zhuohui" uniqKey="Liu Z" first="Zhuohui" last="Liu">Zhuohui Liu</name><name sortKey="Yu, Hualin" sort="Yu, Hualin" uniqKey="Yu H" first="Hualin" last="Yu">Hualin Yu</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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