{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,5]],"date-time":"2026-06-05T02:01:43Z","timestamp":1780624903363,"version":"3.54.1"},"reference-count":81,"publisher":"American Society for Microbiology","issue":"16","license":[{"start":{"date-parts":[[2011,8,15]],"date-time":"2011-08-15T00:00:00Z","timestamp":1313366400000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["J Virol"],"published-print":{"date-parts":[[2011,8,15]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:p>\n            miR-155, processed from the B-cell integration cluster (BIC), is one of the few well-studied microRNAs (miRNAs) and is involved in both innate immunity and tumorigenesis. BIC\/miR-155 is induced by distinct signaling pathways, but little is known about the underlying mechanisms. We have identified two conserved potential interferon (IFN) regulatory factor (IRF)-binding\/interferon-stimulated response element motifs in the\n            <jats:named-content content-type=\"genus-species\">Bic<\/jats:named-content>\n            gene promoter. Two oncogenic IRFs, IRF4 and -7, in addition to some other members of the family, bind to and significantly transactivate the\n            <jats:named-content content-type=\"genus-species\">Bic<\/jats:named-content>\n            promoter. Correspondingly, the endogenous levels of IRF4 and -7 are correlated with that of the BIC transcript in Epstein-Barr virus (EBV)-transformed cells. However, RNA interference studies have shown that depletion of IRF4, rather than of IRF7, dramatically decreases the endogenous level of BIC by up to 70% in EBV- or human T-cell leukemia virus type 1 (HTLV1)-transformed cell lines and results in apoptosis and reduction of proliferation rates that are restored by transient expression of miR-155. Moreover, the endogenous levels of the miR-155 target, SHIP1, are consistently elevated in EBV- and HTLV1-transformed cell lines stably expressing shIRF4. In contrast, transient expression of IRF4 decreases the SHIP1 level in EBV-negative B cells. Furthermore, the level of IRF4 mRNA is significantly correlated with that of BIC in adult T-cell lymphoma\/leukemia (ATLL) tumors. These results show that IRF4 plays an important role in the regulation of BIC in the context of EBV and HTLV1 infection. Our findings have identified\n            <jats:named-content content-type=\"genus-species\">Bic<\/jats:named-content>\n            as the first miRNA-encoding gene for IRFs and provide evidence for a novel molecular mechanism underlying the IRF\/BIC pathway in viral oncogenesis.\n          <\/jats:p>","DOI":"10.1128\/jvi.00570-11","type":"journal-article","created":{"date-parts":[[2011,6,17]],"date-time":"2011-06-17T03:15:39Z","timestamp":1308280539000},"page":"8328-8337","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":48,"title":["Oncogenic IRFs Provide a Survival Advantage for Epstein-Barr Virus- or Human T-Cell Leukemia Virus Type 1-Transformed Cells through Induction of BIC Expression"],"prefix":"10.1128","volume":"85","author":[{"given":"Ling","family":"Wang","sequence":"first","affiliation":[{"name":"Division of Hematology\/Oncology, Viral Oncology 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