期刊
CANCER LETTERS
卷 452, 期 -, 页码 203-212出版社
ELSEVIER IRELAND LTD
DOI: 10.1016/j.canlet.2019.03.025
关键词
Pancreatic cancer; Sulforaphane; NF-kappa B signaling; microRNA
类别
资金
- China Scholarship Council
- German Research Council [DFG HE 3186/15-1]
- Heidelberger Stiftung Chirurgie
- Dietmar Hopp Stiftung
- Hanns A. Pielenz-Stiftung
- Klaus Tschira Stiftung
- German Cancer Aid (Deutsche Krebshilfe) [111299]
NF-kappa B contributes to the aggressiveness of pancreatic ductal adenocarcinoma (PDA), which is counteracted by the bioactive agent sulforaphane. We investigated sulforaphane-induced microRNA signaling and its influence on progression features. Using established cell lines, microRNA and gene arrays, we predicted miR-365a as the top candidate for the sulforaphane-induced inhibition of the NF-kappa B subunit c-Rel. The lipofection of miR-365a-3p mimics inhibited the luciferase activity of a c-Rel 3'-UTR construct, as well as c-Rel expression, NF-kappa B activity, and tumor viability, migration, and clonogenicity, whereas apoptosis was induced. In vivo, miR-365a-3p reduced the volume of tumor xenografts and the expression of progression markers. In a tissue array, the expression of miR-365a-3p was absent in almost all 91 malignant tissues but not in 5 normal tissues, thus confirming the previous results. Our observations suggest that sulforaphane-induced miR-365a-3p expression inhibits NF-kappa B activity by downregulating c-Rel, which prevents the progression of PDA.
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