{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,18]],"date-time":"2026-08-18T00:48:54Z","timestamp":1787014134897,"version":"build-2736575974"},"reference-count":46,"publisher":"Wiley","issue":"6","license":[{"start":{"date-parts":[[2017,9,11]],"date-time":"2017-09-11T00:00:00Z","timestamp":1505088000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/501100001691","name":"Japan Society for the Promotion of Science","doi-asserted-by":"publisher","award":["15K18414"],"award-info":[{"award-number":["15K18414"]}],"id":[{"id":"10.13039\/501100001691","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001691","name":"Japan Society for the Promotion of Science","doi-asserted-by":"publisher","award":["25461428"],"award-info":[{"award-number":["25461428"]}],"id":[{"id":"10.13039\/501100001691","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["European J of Haematology"],"published-print":{"date-parts":[[2017,12]]},"abstract":"Abstract<\/jats:title>\n \n Background<\/jats:title>\n \n Human T\u2010cell leukemia virus type 1 (\n HTLV<\/jats:styled-content>\n \u20101) causes adult T\u2010cell leukemia (\n ATL<\/jats:styled-content>\n ). Viral Tax protein plays a major role in\n ATL<\/jats:styled-content>\n development. Pim family of serine\/threonine kinases is composed of Pim\u20101, \u20102, and \u20103. The potential of Pim family as a target in\n ATL<\/jats:styled-content>\n was analyzed.\n <\/jats:p>\n <\/jats:sec>\n \n Methods<\/jats:title>\n \n RT<\/jats:styled-content>\n \u2010\n PCR<\/jats:styled-content>\n and Western blotting were used to determine the expression of Pim kinases, Tax, and intracellular signal molecules. Knockdown of Pim\u20103 and RelA was performed using small interfering\n RNA<\/jats:styled-content>\n . The effects on cell proliferation, viability, cell cycle, and apoptosis were analyzed by\n WST<\/jats:styled-content>\n \u20108, propidium iodide, and\n APO<\/jats:styled-content>\n 2.7 assay.\n NF<\/jats:styled-content>\n \u2010\u03baB\n DNA<\/jats:styled-content>\n binding activity was investigated by electrophoretic mobility shift assay.\n <\/jats:p>\n <\/jats:sec>\n \n Results<\/jats:title>\n \n Pim\u20103 expression was restricted to\n HTLV<\/jats:styled-content>\n \u20101\u2013infected T\u2010cell lines. Tax induced Pim\u20103 expression through\n NF<\/jats:styled-content>\n \u2010\u03baB. Knockdown of Pim\u20103 showed growth inhibition of\n HTLV<\/jats:styled-content>\n \u20101\u2013infected T cells.\n NJC<\/jats:styled-content>\n 97\u2010\n NH<\/jats:styled-content>\n , a novel inhibitor of the Pim\u20101\/3 kinases, inhibited cell viability.\n NJC<\/jats:styled-content>\n 97\u2010\n NH<\/jats:styled-content>\n induced G2\/M cell cycle arrest associated with downregulation of cyclin A and cyclin B1 expression, as well as apoptosis accompanied with downregulation of\n XIAP<\/jats:styled-content>\n and Mcl\u20101 expression through inhibition of\n NF<\/jats:styled-content>\n \u2010\u03baB pathway, mediated through decrease in I\u03baB\u03b1 and RelA phosphorylation.\n <\/jats:p>\n <\/jats:sec>\n \n Conclusion<\/jats:title>\n \n Pim\u20103 is a potentially suitable target for the development of novel therapeutic agents against\n ATL<\/jats:styled-content>\n .\n <\/jats:p>\n 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