Fetuin B overexpression suppresses proliferation, migration, and invasion in prostate cancer by inhibiting the PI3K/AKT signaling pathway - 28/10/20
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Graphical abstract |
Highlights |
• | FETUB was inversely related to the PSA content. |
• | FETUB was lowly expressed in PCA than in BPH. |
• | FETUB regulates PCA by the PI3K / AKT pathway. |
• | FETUB inhibits tumor growth in nude mice. |
Abstract |
Fetuin B (FETUB) is a glycoprotein that is a member of the cysteine protease inhibitor family, and it is associated with cancer. However, the role of FETUB in prostate carcinogenesis is unknown. In this study, we overexpressed FETUB in prostate cancer cells by using lentivirus and then studied the impacts on cell apoptosis, migration and invasion. We found that apoptosis was increased and the migration and invasion of prostate cancer cells were significantly inhibited after overexpression. Then, we performed experiments in vivo and found that there were fewer tumors in the overexpression groups than in the control groups. In addition, we demonstrated that overexpression of FETUB inactivates the PI3K/AKT signaling pathway. Rescue assays revealed that intervention of 740Y-P reversed the anti-tumor effect of FETUB on prostate cancer cells. Taken together, our results revealed that FETUB may act as a novel regulator to promote apoptosis and inhibit the migration and invasion of prostate cancer cells and that FETUB is related to the inactivation of the PI3K/AKT signaling pathway.
El texto completo de este artículo está disponible en PDF.Keywords : Fetuin B (FETUB), Prostate cancer, PI3K/AKT, Epithelial–mesenchymal transition (EMT)
Esquema
Vol 131
Artículo 110689- novembre 2020 Regresar al número
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