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Deregulated expression of miR-107 inhibits metastasis of PDAC through inhibition PI3K/Akt signaling via caveolin-1 and PTEN.

Deregulated expression of miR-107 inhibits metastasis of PDAC through inhibition PI3K/Akt signaling via caveolin-1 and PTEN.
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Xiong J, Wang D, Wei A, Lu H, Tan C, Li A, Tang J, Wang Y, He S, Liu X, Hu W,


Xiong J, Wang D, Wei A, Lu H, Tan C, Li A, Tang J, Wang Y, He S, Liu X, Hu W, (click to view)

Xiong J, Wang D, Wei A, Lu H, Tan C, Li A, Tang J, Wang Y, He S, Liu X, Hu W,

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Experimental cell research 2017 10 28361(2) 316-323 pii 10.1016/j.yexcr.2017.10.033

Abstract

Pancreatic ductal adenocarcinoma (PDAC) displays a highly aggressive malignancy and is considered to be an incurable and rapidly lethal disease. MicroRNAs (miRNAs) are small non-coding RNAs of approximately nucleotides that regulate several aspects of tumors pathogenesis, including migration, invasion, metastasis and epithelial-mesenchymal transition. We have found that miR-107 was significantly high expression in PDAC tissues and cells. High miR-107 expression is associated with poor clinicopathological parameters and prognosis in PDAC patients. Deregulated expression of miR-107 in PDAC cells (AsPC-1 and Panc-1) is sufficient to reduce cell migration and invasion, and to induce upregulation of epithelial markers (β-catenin, ZO-1 and E-cadherin) and a decrease of mesenchymal marker expression (ZEB-1 and vimentin). We also found that the caveolin-1, PTEN and p-Akt expression are modulated by miR-107 in PDAC cells. Moreover, our study clearly demonstrated that deregulated expression of miR-107 inhibited cell migration and invasion and EMT by up-regulation of caveolin-1 and PTEN, and inhibition of PI3K/Akt signaling in PDAC cells. Our study suggested that miR‑107 expression might both be a useful indicator of the metastatic potential and provided a new potential therapeutic target in PDAC.

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