miR-15a/miR-16 cluster inhibits invasion of prostate cancer cells by suppressing TGF-β signaling pathway - 11/06/18
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Graphical abstract |
Highlights |
• | Overexpression of miR-15a/16 inhibits the TGF-β signaling pathway. |
• | Both Smad3 and ACVR2A are targets of miR-15a/16. |
• | TGF-β pathway-targeting miRNAs are critical in regulating progression and metastasis of prostate cancer. |
Abstract |
Background |
To determine whether and how miR15a/16 regulate TGF-β signaling pathways during the progression of prostate cancer.
Methods |
We used bioinformatics prediction, reporter gene assay, real-time PCR, Matrigel invasion assay and Western blot to dissect the molecular mechanism of how miR-15a/miR-16 may cause metastasis in prostate tumor.
Results |
MiR-15a/16 targeted and inhibited the expression of endogenous Smad3 and ACVR2A proteins. The overexpression of miR15a/16 down-regulated p-smad3 expression, affected the expression of both MMP2 and E-cadherin, and down-regulated the expression of the EMT-mediated factors Snail and Twist in LNCaP prostate cancer cells. The overexpression of miR15a/16 decreased the invasion of LNCaP cells. MiR-15a/miR-16 cluster could reverse the invasion of activin A-mediated prostate cancer cells. After the inhibition of the activin/smad signaling pathway, the inhibitory effect of invasion in prostate cancer cells by miR-15a/miR-16 cluster disappeared.
Conclusion |
Our data indicated that miR15a/16 inhibited the components of TGF-β signaling pathways in LNCaP cell line, which might relate to the progression and metastasis of prostate cancer.
El texto completo de este artículo está disponible en PDF.Keywords : MicroRNAs, miR15a/16, TGF-β signaling pathways, LNCaP cells
Esquema
Vol 104
P. 637-644 - août 2018 Regresar al númeroBienvenido a EM-consulte, la referencia de los profesionales de la salud.
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