{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,12,8]],"date-time":"2025-12-08T22:54:03Z","timestamp":1765234443900},"reference-count":42,"publisher":"Wiley","issue":"12","license":[{"start":{"date-parts":[[2018,10,23]],"date-time":"2018-10-23T00:00:00Z","timestamp":1540252800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/100000054","name":"National Cancer Institute","doi-asserted-by":"publisher","award":["P30 CA043703"],"award-info":[{"award-number":["P30 CA043703"]}],"id":[{"id":"10.13039\/100000054","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["febs.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Molecular Oncology"],"published-print":{"date-parts":[[2018,12]]},"abstract":"<jats:p>Protein inhibitor of activated <jats:styled-content style=\"fixed-case\">STAT<\/jats:styled-content>3 (<jats:styled-content style=\"fixed-case\">PIAS<\/jats:styled-content>3) is an endogenous suppressor of signal transducer and activator of transcription 3 (<jats:styled-content style=\"fixed-case\">STAT<\/jats:styled-content>3) signaling. By directly interacting with phosphorylated <jats:styled-content style=\"fixed-case\">STAT<\/jats:styled-content>3, <jats:styled-content style=\"fixed-case\">PIAS<\/jats:styled-content>3 can block the downstream transcriptional activity of <jats:styled-content style=\"fixed-case\">STAT<\/jats:styled-content>3, which is hyper\u2010activated in various cancers. We previously reported that in malignant mesothelioma (<jats:styled-content style=\"fixed-case\">MM<\/jats:styled-content>), low <jats:styled-content style=\"fixed-case\">PIAS<\/jats:styled-content>3 expression is associated with increased <jats:styled-content style=\"fixed-case\">STAT<\/jats:styled-content>3 activation and correlates with poor patient survival, yet the regulatory mechanism(s) governing <jats:styled-content style=\"fixed-case\">PIAS<\/jats:styled-content>3 expression in <jats:styled-content style=\"fixed-case\">MM<\/jats:styled-content> remain unclear. Here, we demonstrate that <jats:styled-content style=\"fixed-case\">PIAS<\/jats:styled-content>3 protein expression does not correlate with its <jats:styled-content style=\"fixed-case\">mRNA<\/jats:styled-content> level in <jats:styled-content style=\"fixed-case\">MM<\/jats:styled-content> cell lines, indicating that <jats:styled-content style=\"fixed-case\">PIAS<\/jats:styled-content>3 expression is regulated at a post\u2010transcriptional level. Inhibition of proteasomal degradation with <jats:styled-content style=\"fixed-case\">MG<\/jats:styled-content>132 (10\u00a0\u03bc<jats:sc>m<\/jats:sc>) or bortezomib (1\u00a0\u03bc<jats:sc>m<\/jats:sc>), alone and in combination, did not increase <jats:styled-content style=\"fixed-case\">PIAS<\/jats:styled-content>3 protein levels; furthermore, inhibition of protein synthesis by cycloheximide treatment did not decrease <jats:styled-content style=\"fixed-case\">PIAS<\/jats:styled-content>3 levels within 48\u00a0h, suggesting that <jats:styled-content style=\"fixed-case\">PIAS<\/jats:styled-content>3 expression is not actively regulated at a post\u2010translational level. To determine whether mi<jats:styled-content style=\"fixed-case\">RNA<\/jats:styled-content> (miRs) can translationally regulate <jats:styled-content style=\"fixed-case\">PIAS<\/jats:styled-content>3 expression, we combined miR microarray analysis with bioinformatic screening to identify candidate miRs, in <jats:styled-content style=\"fixed-case\">MM<\/jats:styled-content> cell lines with low <jats:styled-content style=\"fixed-case\">PIAS<\/jats:styled-content>3 expression, followed by luciferase reporter assays to validate miR regulation of the <jats:styled-content style=\"fixed-case\">PIAS<\/jats:styled-content>3 3\u2032<jats:styled-content style=\"fixed-case\">UTR<\/jats:styled-content>. We identified miR\u201018a as a suppressor of <jats:styled-content style=\"fixed-case\">PIAS<\/jats:styled-content>3 expression that is upregulated in <jats:styled-content style=\"fixed-case\">MM<\/jats:styled-content> cells and whose inhibition can increase <jats:styled-content style=\"fixed-case\">PIAS<\/jats:styled-content>3 expression and suppress <jats:styled-content style=\"fixed-case\">STAT<\/jats:styled-content>3 activity. Moreover, we showed that miR\u201018a inhibition can decrease <jats:styled-content style=\"fixed-case\">MM<\/jats:styled-content> cell viability and that its expression is negatively correlated with <jats:styled-content style=\"fixed-case\">MM<\/jats:styled-content> patient survival. Taken together, these results suggest that targeting miR\u201018a may have therapeutic benefit in <jats:styled-content style=\"fixed-case\">MM<\/jats:styled-content>.<\/jats:p>","DOI":"10.1002\/1878-0261.12386","type":"journal-article","created":{"date-parts":[[2018,9,27]],"date-time":"2018-09-27T07:09:12Z","timestamp":1538032152000},"page":"2124-2135","update-policy":"http:\/\/dx.doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":15,"title":["Post\u2010transcriptional regulation of <scp>PIAS<\/scp>3 expression by miR\u201018a in malignant mesothelioma"],"prefix":"10.1002","volume":"12","author":[{"given":"Tian","family":"He","sequence":"first","affiliation":[{"name":"Department of Biochemistry School of Medicine, Case Western Reserve University Cleveland OH USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Karen","family":"McColl","sequence":"additional","affiliation":[{"name":"Division of Hematology and Oncology Case Western Reserve 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