{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T08:33:41Z","timestamp":1791275621293,"version":"4.1.0"},"reference-count":51,"publisher":"Portland Press Ltd.","issue":"2","content-domain":{"domain":["portlandpress.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2014,4,15]]},"abstract":"<jats:p>LXR (liver X receptor) is a ligand-activated transcription factor and plays an important role in regulation of lipid homoeostasis and inflammation. Several studies indicate that LXR inhibits IFN-\u03b3 (interferon \u03b3)-induced biological responses; however, the influence of LXR on IFN-\u03b3 expression has not been fully elucidated. In the present study, we investigated the effects of LXR activation on IFN-\u03b3 expression at different levels. At the molecular level, we surprisingly observed that LXR ligand (T0901317) induced macrophage and T-cell IFN-\u03b3 protein expression which was associated with increased mRNA and secreted protein levels in culture medium. In contrast, selective inhibition of LXR\u03b1 and\/or LXR\u03b2 expression by siRNA reduced IFN-\u03b3 expression. Promoter analysis defined the multiple LXREs (LXR-responsive elements) in the proximal region of the IFN-\u03b3 promoter. EMSAs and ChIP indicated that LXR activation enhanced the binding of LXR protein to these LXREs. In\u00a0vivo, T0901317 increased wild-type mouse serum IFN-\u03b3 levels and IFN-\u03b3 expression in the lung and lymph nodes. Functionally, we observed that administration of T0901317 to wild-type mice increased rates of survival and being tumour-free, and inhibited tumour growth when the animals were inoculated with LLC1 carcinoma. In contrast, these protective effects were substantially attenuated in IFN-\u03b3-knockout (IFN-\u03b3\u2212\/\u2212) mice, suggesting that the induction of IFN-\u03b3 production plays a critical role in T0901317-inhibited tumour growth. Taken together, the results of the present study show that IFN-\u03b3 is another molecular target of LXR activation, and it suggests a new mechanism by which LXR inhibits tumour growth.<\/jats:p>","DOI":"10.1042\/bj20131442","type":"journal-article","created":{"date-parts":[[2014,1,21]],"date-time":"2014-01-21T09:27:10Z","timestamp":1390296430000},"page":"345-354","update-policy":"https:\/\/doi.org\/10.1042\/crossmark_policy","source":"Crossref","is-referenced-by-count":36,"title":["Identification of interferon-\u03b3 as a new molecular target of liver X receptor"],"prefix":"10.1042","volume":"459","author":[{"given":"Qixue","family":"Wang","sequence":"first","affiliation":[{"name":"State Key Laboratory of Medicinal Chemical Biology, Nankai University, Tianjin 300071, China"},{"name":"College of Life Sciences, Nankai University, Tianjin 300071, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xingzhe","family":"Ma","sequence":"additional","affiliation":[{"name":"State Key Laboratory of Medicinal Chemical Biology, Nankai University, Tianjin 300071, China"},{"name":"College of Life Sciences, Nankai University, Tianjin 300071, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yuanli","family":"Chen","sequence":"additional","affiliation":[{"name":"College of Life Sciences, Nankai University, Tianjin 300071, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ling","family":"Zhang","sequence":"additional","affiliation":[{"name":"College of Life Sciences, Nankai University, Tianjin 300071, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Meixiu","family":"Jiang","sequence":"additional","affiliation":[{"name":"College of Life Sciences, Nankai University, Tianjin 300071, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xiaoju","family":"Li","sequence":"additional","affiliation":[{"name":"College of Life Sciences, Nankai University, Tianjin 300071, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rong","family":"Xiang","sequence":"additional","affiliation":[{"name":"Collaborative Innovation Center of Biotherapy, Nankai University, Tianjin 300071, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Robert","family":"Miao","sequence":"additional","affiliation":[{"name":"Medical College of Wisconsin, Milwaukee, WI 53213, U.S.A."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"David\u00a0P.","family":"Hajjar","sequence":"additional","affiliation":[{"name":"Weill Cornell Medical College, New York, NY 10065, U.S.A."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yajun","family":"Duan","sequence":"additional","affiliation":[{"name":"State Key Laboratory of Medicinal Chemical Biology, Nankai University, Tianjin 300071, China"},{"name":"Collaborative Innovation Center of Biotherapy, Nankai University, Tianjin 300071, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jihong","family":"Han","sequence":"additional","affiliation":[{"name":"State Key Laboratory of Medicinal Chemical Biology, Nankai University, Tianjin 300071, China"},{"name":"College of Life Sciences, Nankai University, Tianjin 300071, China"},{"name":"Collaborative Innovation Center of Biotherapy, Nankai University, Tianjin 300071, China"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"288","published-online":{"date-parts":[[2014,3,28]]},"reference":[{"key":"2021112215570496900_B1","doi-asserted-by":"crossref","first-page":"556","DOI":"10.1016\/S1471-4906(01)02005-1","article-title":"IFN-\u03b3 production by antigen-presenting cells: mechanisms emerge","volume":"22","author":"Frucht","year":"2001","journal-title":"Trends Immunol."},{"key":"2021112215570496900_B2","doi-asserted-by":"crossref","first-page":"2821","DOI":"10.4049\/jimmunol.131.6.2821","article-title":"Activation of human monocyte cytotoxicity by natural and recombinant immune interferon","volume":"131","author":"Le","year":"1983","journal-title":"J. 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