{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,18]],"date-time":"2026-03-18T22:10:56Z","timestamp":1773871856768,"version":"3.50.1"},"reference-count":41,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2008,11,12]],"date-time":"2008-11-12T00:00:00Z","timestamp":1226448000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Journal Cellular Physiology"],"published-print":{"date-parts":[[2009,3]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>The constitutively active Bcr\u2010Abl tyrosine kinase plays a crucial role in chronic myelogenous leukemia (CML) pathogenesis. The Bcr\u2010Abl protein induces the upregulation of proto\u2010oncogene c\u2010Jun, which is involved in Bcr\u2010Abl transforming activity in Bcr\u2010Abl positive cells. Recent studies reported that c\u2010Jun inhibited hemoglobin synthesis in human CML cell line K562. However, c\u2010Jun also plays a critical role in cell proliferation and apoptosis. In this study, we investigated the physiological roles of c\u2010Jun in cell proliferation, apoptosis and erythroid differentiation of K562 cells. Firstly, we generated K562 cell lines stably overexpressing c\u2010Jun. These clones have the same proliferation rate as the parental cell line in general culture medium. Endogenous c\u2010Jun expression was analyzed to determine the effective concentration of STI571 for inhibiting Bcr\u2010Abl signaling. Western blots show that STI571 inhibited c\u2010Jun expression in a dose\u2010dependent manner, reaching a maximum inhibition at 1 \u00b5M. STI571 could inhibit c\u2010Jun expression in K562 cells, but not in c\u2010Jun\u2010overexpression cells. c\u2010Jun did not alter growth inhibition and apoptotic induction by STI571 treatment, but inhibited STI571\u2010induced erythroid differentiation. Moreover, c\u2010Jun did not alter growth inhibition and apoptotic induction by histone deacetylase (HDAC) inhibitors (apicidin, sodium butyrate, and MS275) treatment, but inhibited HDAC inhibitors\u2010induced erythroid differentiation. These results suggest that c\u2010Jun may modulate anticancer drugs\u2010induced cell differentiation but not growth inhibition and apoptosis in CML cells. J. Cell. Physiol. 218: 568\u2013574, 2009. \u00a9 2008 Wiley\u2010Liss, Inc.<\/jats:p>","DOI":"10.1002\/jcp.21627","type":"journal-article","created":{"date-parts":[[2008,11,12]],"date-time":"2008-11-12T13:50:24Z","timestamp":1226497824000},"page":"568-574","source":"Crossref","is-referenced-by-count":12,"title":["c\u2010Jun blocks cell differentiation but not growth inhibition or apoptosis of chronic myelogenous leukemia cells induced by STI571 and by histone deacetylase inhibitors"],"prefix":"10.1002","volume":"218","author":[{"given":"Huei\u2010Mei","family":"Huang","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Juo\u2010Chuan","family":"Liu","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[2008,11,12]]},"reference":[{"key":"e_1_2_6_2_1","doi-asserted-by":"publisher","DOI":"10.1128\/MCB.11.12.6286"},{"key":"e_1_2_6_3_1","doi-asserted-by":"publisher","DOI":"10.1126\/science.3460176"},{"key":"e_1_2_6_4_1","doi-asserted-by":"publisher","DOI":"10.1182\/blood-2002-09-2896"},{"key":"e_1_2_6_5_1","first-page":"877","article-title":"Suppression of oncogene\u2010induced transformation by a deletion mutant of c\u2010jun","volume":"8","author":"Brown PH","year":"1992","journal-title":"Oncogene"},{"key":"e_1_2_6_6_1","first-page":"100","article-title":"Inhibition of the Abl protein\u2010tyrosine kinase in vitro and in 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