{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Hu YL"],"funding":["China Postdoctoral Science Foundation","National Natural Science Foundation of China","Jiangsu Postdoctoral Research Foundation","Nantong Science and Technology Bureau","Three-Side Innovation Projects for Aquaculture in Jiangsu Province","Jiangsu Provincial Medical Youth Talent"],"pagination":["7637-7651"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC7339162"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["24(13)"],"pubmed_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."],"journal":["Journal of cellular and molecular medicine"],"pubmed_title":["SNHG16/miR-605-3p/TRAF6/NF-κB feedback loop regulates hepatocellular carcinoma metastasis."],"pmcid":["PMC7339162"],"funding_grant_id":["2016M590489","2017T100393","81672409","QNRC2016700","MSZ19203","1601101C","MSZ19204","BRA2018394","MS12019026"],"pubmed_authors":["Xue WJ","Liu JZ","Feng Y","Huang H","Mao QS","Chen YY","Li P","Hu YL","Su Y"],"additional_accession":[]},"is_claimable":false,"name":"SNHG16/miR-605-3p/TRAF6/NF-κB feedback loop regulates hepatocellular carcinoma metastasis.","description":"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.","dates":{"release":"2020-01-01T00:00:00Z","publication":"2020 Jul","modification":"2025-05-29T19:52:47.096Z","creation":"2025-05-29T19:52:47.096Z"},"accession":"S-EPMC7339162","cross_references":{"pubmed":["32436333"],"doi":["10.1111/jcmm.15399"]}}