{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,7]],"date-time":"2026-10-07T00:46:56Z","timestamp":1791334016502,"version":"4.3.1"},"reference-count":62,"publisher":"American Society of Hematology","issue":"3","content-domain":{"domain":["ashpublications.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2002,8,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>In epithelial cells \u03b2-catenin plays a critical role as a component of the cell-cell adhesion apparatus and as a coactivator of the TCF\/LEF (T-cell transcription factor\/lymphoid enhancer binding factor) family of transcription factors. Deregulation of \u03b2-catenin has been implicated in the malignant transformation of cells of epithelial origin. However, a function for \u03b2-catenin in hematologic malignancies has not been reported. \u03b2-Catenin is not detectable in normal peripheral blood T cells but is expressed in T\u2013acute lymphoblastic leukemia cells and other tumor lines of hematopoietic origin and in primary lymphoid and myeloid leukemia cells. \u03b2-Catenin function was examined in Jurkat T\u2013acute lymphoblastic leukemia cells. Overexpression of dominant-negative \u03b2-catenin or dominant-negative TCF reduced \u03b2-catenin nuclear signaling and inhibited Jurkat proliferation and clonogenicity. Similarly, these constructs inhibited proliferation of K562 and HUT-102 cells. Reduction of \u03b2-catenin expression with \u03b2-catenin antisense down-regulated adhesion of Jurkat cells in response to phytohemagglutinin. Incubation of Jurkat cells with anti-Fas induced caspase-dependent limited proteolysis of \u03b2-catenin N- and C-terminal regions and rapid redistribution of \u03b2-catenin to the detergent-insoluble cytoskeleton, concomitant with a marked decline in nuclear \u03b2-catenin signaling. Fas-mediated apoptosis was potentiated by inhibition of \u03b2-catenin nuclear signaling. The data suggest that \u03b2-catenin can play a significant role in promoting leukemic cell proliferation, adhesion, and survival.<\/jats:p>","DOI":"10.1182\/blood.v100.3.982","type":"journal-article","created":{"date-parts":[[2002,10,11]],"date-time":"2002-10-11T18:33:52Z","timestamp":1034361232000},"page":"982-990","update-policy":"https:\/\/doi.org\/10.1182\/blood.2019cm0000","source":"Crossref","is-referenced-by-count":105,"title":["Regulation of leukemic cell adhesion, proliferation, and survival by \u03b2-catenin"],"prefix":"10.1182","volume":"100","author":[{"given":"Eun Joo","family":"Chung","sequence":"first","affiliation":[{"name":"From the Medical Oncology Clinical Research Unit and Developmental Therapeutics Program; Experimental Immunology Branch; and Laboratory of Cellular and Molecular Biology; all of the National Cancer Institute, National Institutes of Health, Bethesda, MD; and Greenebaum Cancer Center, University of Maryland, Baltimore."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sang-Gu","family":"Hwang","sequence":"additional","affiliation":[{"name":"From the Medical Oncology Clinical Research Unit and Developmental Therapeutics Program; Experimental Immunology Branch; and Laboratory of Cellular and Molecular Biology; all of the National Cancer Institute, National Institutes of Health, Bethesda, MD; and Greenebaum Cancer Center, University of Maryland, Baltimore."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"PhuongMai","family":"Nguyen","sequence":"additional","affiliation":[{"name":"From the Medical Oncology Clinical Research Unit and Developmental Therapeutics Program; Experimental Immunology Branch; and Laboratory of Cellular and Molecular Biology; all of the National Cancer Institute, National Institutes of Health, Bethesda, MD; and Greenebaum Cancer Center, University of Maryland, 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