{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Luce A"],"funding":["Epimet","PNRR - MISSIONE 4 COMPONENTE 2 \"Dalla Ricerca all'Impresa\".e"],"pagination":["1008"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12462032"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["23(1)"],"pubmed_abstract":["<h4>Background</h4>Hepatocellular carcinoma (HCC) remains a significant clinical challenge due to limited diagnostic and therapeutic options. Non-coding RNAs (ncRNAs), such as microRNAs (miRNAs), play key roles in cancer biology. Our previous findings showed that miR-423-5p enhances anti-cancer effects on HCC patients treated with sorafenib by promoting autophagy. Here, we investigated the molecular mechanisms underlying miR-423-5p function through a comprehensive proteomic approach.<h4>Methods</h4>We generated an HCC cell line stably overexpressing miR-423-5p via lentiviral transduction. Total proteins were extracted from SNU-387 cells, enzymatically digested into peptides, and subsequently analysed by liquid chromatography-tandem mass spectrometry (LC-MS/M). Raw spectral data were proces"],"journal":["Journal of translational medicine"],"pubmed_title":["Proteomic profiling identifies miR-423-5p as a modulator of oncogenic metabolism in HCC."],"pmcid":["PMC12462032"],"funding_grant_id":["(PE00000019)","(F/310034/03/X56)"],"pubmed_authors":["Luce A","Boocock DJ","Tathode MS","Coveney C","Verderio EAM","Cossu AM","Zappavigna S","Romano MP","Misso G","Vitale G","Sperlongano R","Caraglia M","De Iesu MR","Simeone I","Mele L","Bocchetti M"],"additional_accession":[]},"is_claimable":false,"name":"Proteomic profiling identifies miR-423-5p as a modulator of oncogenic metabolism in HCC.","description":"<h4>Background</h4>Hepatocellular carcinoma (HCC) remains a significant clinical challenge due to limited diagnostic and therapeutic options. Non-coding RNAs (ncRNAs), such as microRNAs (miRNAs), play key roles in cancer biology. Our previous findings showed that miR-423-5p enhances anti-cancer effects on HCC patients treated with sorafenib by promoting autophagy. Here, we investigated the molecular mechanisms underlying miR-423-5p function through a comprehensive proteomic approach.<h4>Methods</h4>We generated an HCC cell line stably overexpressing miR-423-5p via lentiviral transduction. Total proteins were extracted from SNU-387 cells, enzymatically digested into peptides, and subsequently analysed by liquid chromatography-tandem mass spectrometry (LC-MS/M). Raw spectral data were proces","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Sep","modification":"2026-07-15T06:48:46.653Z","creation":"2026-06-30T03:23:27.538Z"},"accession":"S-EPMC12462032","cross_references":{"pubmed":["40993657"],"doi":["10.1186/s12967-025-07039-4"]}}