{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,11]],"date-time":"2026-09-11T01:40:11Z","timestamp":1789090811733,"version":"build-2803163510"},"reference-count":54,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2025,1,23]],"date-time":"2025-01-23T00:00:00Z","timestamp":1737590400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["J Neuroendocrinology"],"published-print":{"date-parts":[[2025,4]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>\n                    Gonadotroph neuroendocrine pituitary tumors are among the most common intracranial neoplasms. A notable proportion of these tumors is characterized by invasive growth which hampers the treatment results and worsens prognoses of patients. Increased hsa\u2010miR\u2010184 expression was observed in invasive as compared to non\u2010invasive gonadotroph tumors. This study aimed to determine the role of hsa\u2010miR\u2010184 expression in invasive growth of gonadotroph tumors. QRT\u2010PCR and bisulfite pyrosequencing were used for evaluating hsa\u2010miR\u2010184 expression and\n                    <jats:italic>MIR184<\/jats:italic>\n                    DNA methylation levels, respectively, in tumors\u00a0and normal pituitary samples. L\u03b2T2 and \u03b1T3\u20101 gonadotroph cells were used to test the effect of miR\u2010184 on cell viability (MTT test), proliferation (BrdU incorporation), and migration (scratch assay). RNA sequencing was applied for transcriptome profiling in miR\u2010184\u2010treated and untreated L\u03b2T2 cells. Differential genes expression analysis combined with target prediction served for identification of\u00a0miR\u2010184 targets. MiRNA\u2010mRNA interaction was subsequently validated with Luciferase reporter assay. Analysis of tissue samples showed that hsa\u2010miR\u2010184 is upregulated in gonadotroph tumors and its expression is higher in invasive than in noninvasive ones. Promoter of\n                    <jats:italic>MIR184<\/jats:italic>\n                    is demethylated in\u00a0tumors, and the methylation level is negatively correlated with hsa\u2010miR\u2010184 expression. Transfecting L\u03b2T2 and \u03b1T3\u20101 with miR\u2010184 mimic resulted in increased cellular proliferation and viability. Differentially expressed genes were identified when comparing miR\u2010184\u2010treated and untreated cells, including\n                    <jats:italic>Nus1<\/jats:italic>\n                    as the only predicted miR\u2010184 target. The interaction between miR\u2010184 and 3'UTR of\n                    <jats:italic>Nus1<\/jats:italic>\n                    was confirmed in vitro in both L\u03b2T2 and \u03b1T3\u20101. Overexpression of Nus1 resulted in lowering cell viability in both cell lines and proliferation in L\u03b2T2. The expression level of\n                    <jats:italic>NUS1<\/jats:italic>\n                    was lower in invasive than in noninvasive tumors. Our results indicate that DNA hypomethylation\u2010related increase of hsa\u2010mir\u2010184 expression contributes to invasive growth of gonadotroph pituitary tumors through targeting\n                    <jats:italic>NUS1,<\/jats:italic>\n                    being one of the various molecular mechanisms involved in conferring aggressive growth potential.\n                  <\/jats:p>","DOI":"10.1111\/jne.13492","type":"journal-article","created":{"date-parts":[[2025,1,23]],"date-time":"2025-01-23T05:37:00Z","timestamp":1737610620000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":4,"title":["<scp>DNA<\/scp>\n                    hypomethylation\u2010related expression of hsa\u2010\n                    <scp>miR<\/scp>\n                    \u2010184 contributes to invasive growth of gonadotroph neuroendocrine pituitary tumors"],"prefix":"10.1111","volume":"37","author":[{"given":"Biniyam","family":"Tsegaye","sequence":"first","affiliation":[{"name":"Department of Molecular and Translational Oncology Maria Sklodowska\u2010Curie National Research Institute of Oncology  Warsaw Poland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Paulina","family":"Kober","sequence":"additional","affiliation":[{"name":"Department of Molecular and Translational Oncology Maria Sklodowska\u2010Curie National Research Institute of Oncology  Warsaw Poland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Beata Joanna","family":"Mossakowska","sequence":"additional","affiliation":[{"name":"Department of Molecular and Translational Oncology Maria Sklodowska\u2010Curie National Research Institute of Oncology  Warsaw Poland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Szymon","family":"Baluszek","sequence":"additional","affiliation":[{"name":"Department of Molecular and 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Poland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-5826-8446","authenticated-orcid":false,"given":"Mateusz","family":"Bujko","sequence":"additional","affiliation":[{"name":"Department of Molecular and Translational Oncology Maria Sklodowska\u2010Curie National Research Institute of Oncology  Warsaw 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