<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Luce A</submitter><funding>Epimet</funding><funding>PNRR - MISSIONE 4 COMPONENTE 2 "Dalla Ricerca all'Impresa".e</funding><pagination>1008</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC12462032</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>23(1)</volume><pubmed_abstract>&lt;h4>Background&lt;/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.&lt;h4>Methods&lt;/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</pubmed_abstract><journal>Journal of translational medicine</journal><pubmed_title>Proteomic profiling identifies miR-423-5p as a modulator of oncogenic metabolism in HCC.</pubmed_title><pmcid>PMC12462032</pmcid><funding_grant_id>(PE00000019)</funding_grant_id><funding_grant_id>(F/310034/03/X56)</funding_grant_id><pubmed_authors>Luce A</pubmed_authors><pubmed_authors>Boocock DJ</pubmed_authors><pubmed_authors>Tathode MS</pubmed_authors><pubmed_authors>Coveney C</pubmed_authors><pubmed_authors>Verderio EAM</pubmed_authors><pubmed_authors>Cossu AM</pubmed_authors><pubmed_authors>Zappavigna S</pubmed_authors><pubmed_authors>Romano MP</pubmed_authors><pubmed_authors>Misso G</pubmed_authors><pubmed_authors>Vitale G</pubmed_authors><pubmed_authors>Sperlongano R</pubmed_authors><pubmed_authors>Caraglia M</pubmed_authors><pubmed_authors>De Iesu MR</pubmed_authors><pubmed_authors>Simeone I</pubmed_authors><pubmed_authors>Mele L</pubmed_authors><pubmed_authors>Bocchetti M</pubmed_authors></additional><is_claimable>false</is_claimable><name>Proteomic profiling identifies miR-423-5p as a modulator of oncogenic metabolism in HCC.</name><description>&lt;h4>Background&lt;/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.&lt;h4>Methods&lt;/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</description><dates><release>2025-01-01T00:00:00Z</release><publication>2025 Sep</publication><modification>2026-07-15T06:48:46.653Z</modification><creation>2026-06-30T03:23:27.538Z</creation></dates><accession>S-EPMC12462032</accession><cross_references><pubmed>40993657</pubmed><doi>10.1186/s12967-025-07039-4</doi></cross_references></HashMap>