{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,2]],"date-time":"2026-06-02T04:13:36Z","timestamp":1780373616579,"version":"3.54.1"},"reference-count":64,"publisher":"The Endocrine Society","issue":"4","license":[{"start":{"date-parts":[[2019,12,25]],"date-time":"2019-12-25T00:00:00Z","timestamp":1577232000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/journals\/pages\/open_access\/funder_policies\/chorus\/standard_publication_model"}],"funder":[{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["R01 HD094378-04"],"award-info":[{"award-number":["R01 HD094378-04"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["R01 ES 028615-02"],"award-info":[{"award-number":["R01 ES 028615-02"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["R01 HD094378-02S1"],"award-info":[{"award-number":["R01 HD094378-02S1"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["R01 HD100367-01"],"award-info":[{"award-number":["R01 HD100367-01"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["U54 MD007602"],"award-info":[{"award-number":["U54 MD007602"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["R01 HD094380-02"],"award-info":[{"award-number":["R01 HD094380-02"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2020,4,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:sec>\n                  <jats:title>Context<\/jats:title>\n                  <jats:p>Uterine fibroids (UF) are the most common benign tumor of the myometrium (MM) in women of reproductive age. However, the mechanism underlying the pathogenesis of UF is largely unknown.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Objective<\/jats:title>\n                  <jats:p>To explore the link between nuclear \u03b2-catenin and UF phenotype and \u03b2-catenin crosstalk with estrogen and histone deacetylases (HDACs).<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Design<\/jats:title>\n                  <jats:p>Protein\/RNA levels of \u03b2-catenin (CTNNB1 gene), its responsive markers cyclin D1 and c-Myc, androgen receptor (AR), p27, and class-I HDACs were measured in matched UF\/MM tissues or cell populations. The effects of chemical inhibition\/activation and genetic knockdown of CTNNB1 on UF phenotype were measured. The anti-UF effect of 2 HDAC inhibitors was evaluated.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Main Outcome Measure<\/jats:title>\n                  <jats:p>\u03b2-catenin nuclear translocation in response to \u03b2-catenin inhibition\/activation, estrogen, and HDAC inhibitors in UF cells.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Results<\/jats:title>\n                  <jats:p>UF tissues\/cells showed significantly higher expression of nuclear \u03b2-catenin, cyclin D1, c-Myc, and HDACs 1, 2, 3, and 8 than MM. Estradiol induced \u03b2-catenin nuclear translocation and consequently its responsive genes in both MM and UF cells, while an estrogen receptor antagonist reversed this induction effect. Treatment with \u03b2-catenin or HDAC inhibitors led to dose-dependent growth inhibition, while Wnt3a treatment increased proliferation compared with control. Chemical inhibition of \u03b2-catenin decreased cyclin D1 and c-Myc expression levels, while \u03b2-catenin activation increased expression of the same markers. Genetic knockdown of CTNNB1 resulted in a marked decrease in \u03b2-catenin, cyclin D1, c-Myc, and AR expression. Treatment of UF cells with HDAC inhibitors decreased nuclear \u03b2-catenin, cyclin D1, and c-Myc expression. Moreover, HDAC inhibitors induced apoptosis of UF cells and cell cycle arrest.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Conclusion<\/jats:title>\n                  <jats:p>\u03b2-catenin nuclear translocation contributes to UF phenotype, and \u03b2-catenin signaling is modulated by estradiol and HDAC activity.<\/jats:p>\n               <\/jats:sec>","DOI":"10.1210\/clinem\/dgz227","type":"journal-article","created":{"date-parts":[[2019,11,25]],"date-time":"2019-11-25T08:40:31Z","timestamp":1574671231000},"page":"e1517-e1535","source":"Crossref","is-referenced-by-count":41,"title":["Activation of \u03b2-Catenin Signaling and its Crosstalk With Estrogen and Histone Deacetylases in Human Uterine Fibroids"],"prefix":"10.1210","volume":"105","author":[{"given":"Mohamed","family":"Ali","sequence":"first","affiliation":[{"name":"Department of Obstetrics and Gynecology, University of Illinois at Chicago, Chicago, Illinois"},{"name":"Department of Surgery, University of Illinois at Chicago, Chicago, Illinois"},{"name":"Clinical Pharmacy Department, Faculty of Pharmacy, ASU, Cairo, Egypt"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sara Mahmoud","family":"Shahin","sequence":"additional","affiliation":[{"name":"Clinical Pharmacy Department, Faculty of Pharmacy, ASU, Cairo, Egypt"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nagwa Ali","family":"Sabri","sequence":"additional","affiliation":[{"name":"Clinical Pharmacy Department, Faculty of Pharmacy, ASU, Cairo, Egypt"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ayman","family":"Al-Hendy","sequence":"additional","affiliation":[{"name":"Department of Obstetrics and Gynecology, University of Illinois at Chicago, Chicago, Illinois"},{"name":"Department of Surgery, University of Illinois at Chicago, Chicago, Illinois"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-7131-8946","authenticated-orcid":false,"given":"Qiwei","family":"Yang","sequence":"additional","affiliation":[{"name":"Department of Obstetrics and Gynecology, University of Illinois at Chicago, Chicago, Illinois"},{"name":"Department of Surgery, University of Illinois at Chicago, Chicago, Illinois"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"80","published-online":{"date-parts":[[2019,12,25]]},"reference":[{"key":"2021122210031363600_CIT0001","doi-asserted-by":"crossref","first-page":"16043","DOI":"10.1038\/nrdp.2016.43","article-title":"Uterine fibroids","volume":"2","author":"Stewart","year":"2016","journal-title":"Nat Rev Dis Primers."},{"issue":"3","key":"2021122210031363600_CIT0002","doi-asserted-by":"crossref","first-page":"337","DOI":"10.1093\/biolre\/iox094","article-title":"Selective progesterone receptor modulators for fertility preservation in women 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