{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T00:13:14Z","timestamp":1791245594516,"version":"4.1.0"},"reference-count":64,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,4,20]],"date-time":"2026-04-20T00:00:00Z","timestamp":1776643200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Cell Dev. Biol."],"abstract":"<jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Metabolic dysfunction\u2013associated steatotic liver disease (MASLD) is an important inducer of hepatocellular carcinoma (HCC). MicroRNAs are key regulators of tumorigenesis. Among these, miR-26a-5p is known to be associated with liver pathogenesis, yet its role in linking MASLD progression to HCC development remains incompletely understood.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>Hepatic miR-26a-5p expression was quantified in the C57BL\/6 mice with a 3-month high-carbohydrate diet (HCD). Public transcriptomic datasets with MASLD and HCC samples were analyzed to identify predicted miR-26a-5p downstream candidates upregulated in the above-mentioned diseases. Associations with tumor features were examined, and protein expression of \u03b2-catenin, c-MYC and EpCAM were evaluated after miR-26a-5p modulation.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Integrative bioinformatics identified miR-26a-5p as a candidate prognostic indicator for metabolic liver disease progression.\n                      <jats:italic>In vivo<\/jats:italic>\n                      , results confirmed that suppressed miR-26a-5p expression is a hallmark of diet-induced metabolic perturbation. Mechanistically,\n                      <jats:italic>in vitro<\/jats:italic>\n                      modulation of miR-26a-5p attenuated oncogenic signaling via the \u03b2-catenin\/c-Myc\/EpCAM axis, establishing its role as a tumor suppressor. Notably,\n                      <jats:italic>in silico<\/jats:italic>\n                      analysis of HCC tissues revealed that high miR-26a-5p levels correlate with enhanced antitumor immunity. Leveraging these insights, we constructed a transcriptional signature from miR-26a-5p downstream candidates and MASLD-HCC differentially expressed genes. This signature effectively stratifies MASLDpatients, discriminating molecular risk groups associated with progression to HCC.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>Integrating transcriptomic, clinical and experimental data suggests the role of miR-26a-5p, along with the MASLD-HCC gene signature (EpCAM, DTNA, and KPNA2), may serve as an early molecular indicator and mechanistic modulator of hepatocarcinogenesis, warranting further functional investigation.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.3389\/fcell.2026.1805025","type":"journal-article","created":{"date-parts":[[2026,4,20]],"date-time":"2026-04-20T05:25:23Z","timestamp":1776662723000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":1,"title":["Integrative transcriptomic analysis reveals miR-26a-5p downregulation and a potential predictive gene signature for the progression of metabolic liver disease"],"prefix":"10.3389","volume":"14","author":[{"given":"Andrei","family":"Sorop","sequence":"first","affiliation":[{"name":"Center of Excellence in Translational Medicine, Fundeni Clinical Institute","place":["Bucharest, Romania"]},{"name":"University of Medicine and Pharmacy \u201cCarol Davila\u201d","place":["Bucharest, Romania"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alina-Veronica","family":"Ghionescu","sequence":"additional","affiliation":[{"name":"Center of Excellence in Translational Medicine, Fundeni Clinical Institute","place":["Bucharest, Romania"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Diana","family":"Larisa Ancu\u021ba","sequence":"additional","affiliation":[{"name":"Center of Excellence in Translational Medicine, Fundeni Clinical Institute","place":["Bucharest, Romania"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Maria-Gabriela","family":"Croitoru","sequence":"additional","affiliation":[{"name":"Center of Excellence in Translational Medicine, Fundeni Clinical Institute","place":["Bucharest, Romania"]},{"name":"Faculty of Biology, University of Bucharest","place":["Bucharest, Romania"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Cristin","family":"Coman","sequence":"additional","affiliation":[{"name":"Center of Excellence in Translational Medicine, Fundeni Clinical Institute","place":["Bucharest, Romania"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Daniela","family":"Lixandru","sequence":"additional","affiliation":[{"name":"Center of Excellence in Translational Medicine, Fundeni Clinical Institute","place":["Bucharest, Romania"]},{"name":"University of Medicine and Pharmacy \u201cCarol Davila\u201d","place":["Bucharest, Romania"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Simona Olimpia","family":"Dima","sequence":"additional","affiliation":[{"name":"Center of Excellence in Translational Medicine, Fundeni Clinical Institute","place":["Bucharest, Romania"]},{"name":"University of Medicine and Pharmacy \u201cCarol Davila\u201d","place":["Bucharest, Romania"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1965","published-online":{"date-parts":[[2026,4,20]]},"reference":[{"key":"B1","doi-asserted-by":"publisher","first-page":"8515343","DOI":"10.1155\/2018\/8515343","article-title":"miR-26a potentially contributes to the regulation of fatty acid and sterol metabolism in vitro human HepG2 cell model of nonalcoholic Fatty liver disease","volume":"2018","author":"Ali","year":"2018","journal-title":"Oxid. 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