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• W3026341390 endingPage "7651" @default.
• W3026341390 startingPage "7637" @default.
• W3026341390 abstract "The mechanism by which miR-605-3p regulates hepatocellular carcinoma (HCC) metastasis has not been clarified. In this study, we found that miR-605-3p was down-regulated in HCC and that low miR-605-3p expression was associated with tumour thrombus and tumour satellites. HCC patients with low miR-605-3p expression showed shorter overall survival and disease-free survival after surgery. Overexpression of miR-605-3p inhibited epithelial-mesenchymal transition and metastasis of HCC through NF-κB signalling by directly inhibiting expression of TRAF6, while silencing of miR-605-3p had the opposite effect. We also found that SNHG16 directly bound to miR-605-3p as a competing endogenous RNA. Mechanistically, high expression of SNHG16 promoted binding to miR-605-3p and inhibited its activity, which led to up-regulation of TRAF6 and sustained activation of the NF-κB pathway, which in turn promoted epithelial-mesenchymal transition and metastasis of HCC. TRAF6 increased SNHG16 promoter activity by activating NF-κB, thereby promoting the transcriptional expression of SNHG16 and forming a positive feedback loop that aggravated HCC malignancy. Our findings reveal a mechanism for the sustained activation of the SNHG16/miR-605-3p/TRAF6/NF-κB feedback loop in HCC and provide a potential target for a new HCC treatment strategy." @default.
• W3026341390 created "2020-05-29" @default.
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• W3026341390 date "2020-05-20" @default.
• W3026341390 modified "2023-10-15" @default.
• W3026341390 title "<i>SNHG16</i> / <i>miR‐605‐3p</i> / <i>TRAF6</i> /NF‐κB feedback loop regulates hepatocellular carcinoma metastasis" @default.
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• W3026341390 doi "https://doi.org/10.1111/jcmm.15399" @default.
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