{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,26]],"date-time":"2026-08-26T22:47:09Z","timestamp":1787784429988,"version":"build-2784847793"},"reference-count":33,"publisher":"Wiley","issue":"6","license":[{"start":{"date-parts":[[2004,2,5]],"date-time":"2004-02-05T00:00:00Z","timestamp":1075939200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Intl Journal of Cancer"],"published-print":{"date-parts":[[2004,5,10]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Deletion on the short arm of chromosome 3 is one of the most important genetic abnormalities in the tumorigenesis of nasopharyngeal carcinoma (NPC). Both physical mapping and functional studies have targeted an NPC\u2010related tumor suppressor gene(s) to chromosome 3p21.3. We have reported recently that <jats:italic>RASSF1A<\/jats:italic> gene, located on a 120\u2010kb minimal deletion region on 3p21.3, was frequently inactivated by promoter hypermethylation in NPC. We further confirmed that <jats:italic>RASSF1A<\/jats:italic> is the critical target tumor suppressor from 3p21.3, with the evidence that loss of expression and aberrant methylation of the other 8 candidate genes\/transcripts (<jats:italic>HYAL2<\/jats:italic>, <jats:italic>FUS1<\/jats:italic>, <jats:italic>RASSF1C<\/jats:italic>, <jats:italic>BLU<\/jats:italic>, <jats:italic>NPRL2<\/jats:italic>, <jats:italic>101F6<\/jats:italic>, <jats:italic>PL6<\/jats:italic> and <jats:italic>CACNA2D2<\/jats:italic>) in this 120\u2010kb region were rare in NPC samples. The contribution of <jats:italic>RASSF1A<\/jats:italic> in NPC tumorigenesis was investigated by restoring its expression in a <jats:italic>RASSF1A<\/jats:italic> deficient cell line, C666\u20101. Transient transfection of wild\u2010type <jats:italic>RASSF1A<\/jats:italic> resulted in marked growth inhibition in NPC cells. Isolated stable clones expressing wild\u2010type <jats:italic>RASSF1A<\/jats:italic> demonstrated retarded cell proliferation <jats:italic>in vitro<\/jats:italic>. Soft\u2010agar assay also showed decreased number and sizes of colony formed in these clones. <jats:italic>In vivo<\/jats:italic> nude mice assay demonstrated the dramatic reduction of tumorigenic potential in the <jats:italic>RASSF1A<\/jats:italic>\u2010transfected clones. Our results provide strong evidence to support <jats:italic>RASSF1A<\/jats:italic> as a target tumor suppressor gene on 3p21.3 in NPC. \u00a9 2004 Wiley\u2010Liss, Inc.<\/jats:p>","DOI":"10.1002\/ijc.20079","type":"journal-article","created":{"date-parts":[[2004,3,12]],"date-time":"2004-03-12T08:01:33Z","timestamp":1079078493000},"page":"839-847","source":"Crossref","is-referenced-by-count":85,"title":["<i>RASSF1A<\/i> is a target tumor suppressor from 3p21.3 in nasopharyngeal carcinoma"],"prefix":"10.1002","volume":"109","author":[{"given":"Lillian 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