{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,19]],"date-time":"2026-09-19T01:20:35Z","timestamp":1789780835054,"version":"4.0.1"},"reference-count":46,"publisher":"Wiley","issue":"8","license":[{"start":{"date-parts":[[2014,4,25]],"date-time":"2014-04-25T00:00:00Z","timestamp":1398384000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["faseb.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["The FASEB Journal"],"published-print":{"date-parts":[[2014,8]]},"abstract":"<jats:p>\n                    Hepatocellular carcinoma (HCC) is a common cancer associated with chronic hepatitis B virus (HBV) infection. Conventional interferon\u2010\u03b1 (IFN\u2010\u03b1) and pegylated IFNs (PEG\u2010IFNs) approved for chronic HBV infection treatment can reduce the risk of HCC but are not suitable for the majority of patients and cause significant side effects. IFN\u2010\u03bb1 is a type III IFN with antiviral, antiproliferative, and immunomodulatory functions similar to type I IFNs but with fewer side effects. However, the tolerability and antitumor activity of PEG\u2010IFN\u2010\u03bb1 in HCC xenograft mice are unknown.\n                    <jats:italic>In vitro<\/jats:italic>\n                    IFN\u2010\u03bb1 treatment of Hep3B and Huh7 human hepatoma cell lines increased MHC class I expression, activated JAK\u2010STAT signaling pathways, induced IFN\u2010stimulated gene expression, and inhibited hepatitis B surface antigen (HBsAg) expression. IFN\u2010\u03bb1 treatment also caused 23.2 and 19.9% growth inhibition of Hep3B and Huh7 cells, respectively, and promoted cellular apoptosis. PEG\u2010IFN\u2010\u03bb1, but not IFN\u2010\u03bb1 treatment, significantly suppressed tumor growth\n                    <jats:italic>(P<\/jats:italic>\n                    = 0.002) and induced tumor cell apoptosis in a Hep3B cell xenograft mouse model without significant weight loss or toxicity. PEG\u2010IFN\u2010\u03bb1 also significantly inhibited\n                    <jats:italic>(P<\/jats:italic>\n                    = 0.000) serum HBsAg secretion from Hep3B xenograft tumors\n                    <jats:italic>in vivo.<\/jats:italic>\n                    Thus, PEG\u2010IFN\u2010\u03bb1 can suppress Hep3B xenograft tumor growth and inhibit HBsAg production and may be a potential treatment for HBV\u2010related HCC.\u2014Tian, S., Hui, X., Fan, Z., Li, Q., Zhang, J., Yang, X., Ma, X., Huang, B., Chen, D., Chen, H. Suppression of hepatocellular carcinoma proliferation and hepatitis B surface antigen secretion with interferon\u2010\u03bb1 or PEG\u2010interferon\u2010\u03bb1.\n                    <jats:italic>FASEB J.<\/jats:italic>\n                    28, 3528\u20133539 (2014).\n                    <jats:ext-link xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" xlink:href=\"http:\/\/www.fasebj.org\">www.fasebj.org<\/jats:ext-link>\n                  <\/jats:p>","DOI":"10.1096\/fj.14-250704","type":"journal-article","created":{"date-parts":[[2014,4,25]],"date-time":"2014-04-25T22:31:34Z","timestamp":1398465094000},"page":"3528-3539","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":14,"title":["Suppression of hepatocellular carcinoma proliferation and hepatitis B surface antigen secretion with interferon\u2010\u03bb1 or 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