{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,5]],"date-time":"2026-10-05T04:56:13Z","timestamp":1791176173004,"version":"4.1.0"},"reference-count":0,"publisher":"Oxford University Press (OUP)","issue":"11","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2004,11,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Hepatocyte growth factor (HGF)-stimulated Met signaling influences tumor survival, growth and progression, all processes involving the transcription factor NF-\u03baB. NF-\u03baB plays a complex role in the control of survival due to the influence of cellular factors acting downstream. We undertook a comparative investigation of two human breast carcinoma cells with different grades of malignancy and HepG2 hepatoma cells, which present a biphasic response to HGF (proliferation followed by apoptosis). We found evidence that HGF induced gene patterns characteristic of survival rather than apoptosis depending on the cell type. The ability of NF-\u03baB to regulate expression of hypoxia-inducible factor-1\u03b1 (HIF-1\u03b1), a survival\/anti-apoptotic gene in cancer, seemed to be critical. In the HepG2 and MCF-7 (low invasive breast carcinoma) cell lines increased transcription and translation were responsible for HIF-1\u03b1 induction after HGF. The regulation by NF-\u03baB was mainly at the level of the 5\u2032-UTR of the HIF-1\u03b1 message. HIF-1 (\u03b1\/\u03b2 heterodimer) was likely to transactivate Mcl-1, another anti-apoptotic gene. Opposite results were observed in MDA-MB-231 cells (highly invasive breast carcinoma), which have high NF-\u03baB activity, further inducible by HGF, because HIF-1\u03b1 mRNA expression and HIF-1 transactivating capacity were HGF-insensitive while the \u03b1 subunit seemed to be degraded after HGF. However, ornithine decarboxylase (ODC) and heme oxygenase mRNA expression persistently increased. By transiently transfecting two ODC gene reporters we demonstrated that ODC is a target gene of NF-\u03baB in HGF-treated tumor cells. By regulating HIF-1 activity and specific gene expression downstream, NF-\u03baB may influence the survival threshold, with an impact on the fate of carcinoma cells after prolonged HGF treatment.<\/jats:p>","DOI":"10.1093\/carcin\/bgh227","type":"journal-article","created":{"date-parts":[[2004,7,7]],"date-time":"2004-07-07T20:19:09Z","timestamp":1089231549000},"page":"2089-2100","source":"Crossref","is-referenced-by-count":99,"title":["RETRACTED: Hepatocyte growth factor-activated NF-\u03baB regulates HIF-1 activity and ODC\n          expression, implicated in survival, differently in different carcinoma cell\n          lines"],"prefix":"10.1093","volume":"25","author":[{"given":"L.","family":"Tacchini","sequence":"first","affiliation":[{"name":"Institute of General Pathology, University of Milan, Via Luigi Mangiagalli 31, 20133 Milan, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"C.","family":"De Ponti","sequence":"additional","affiliation":[{"name":"Institute of General Pathology, University of Milan, Via Luigi Mangiagalli 31, 20133 Milan, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"E.","family":"Matteucci","sequence":"additional","affiliation":[{"name":"Institute of General Pathology, University of Milan, Via Luigi Mangiagalli 31, 20133 Milan, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"R.","family":"Follis","sequence":"additional","affiliation":[{"name":"Institute of General Pathology, University of Milan, Via Luigi Mangiagalli 31, 20133 Milan, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"M.A.","family":"Desiderio","sequence":"additional","affiliation":[{"name":"Institute of General Pathology, University of Milan, Via Luigi Mangiagalli 31, 20133 Milan, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2004,11,1]]},"container-title":["Carcinogenesis"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/academic.oup.com\/carcin\/article-pdf\/25\/11\/2089\/7511077\/bgh227.pdf","content-type":"application\/pdf","content-version":"vor","intended-application":"syndication"},{"URL":"https:\/\/academic.oup.com\/carcin\/article-pdf\/25\/11\/2089\/7511077\/bgh227.pdf","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2026,9,9]],"date-time":"2026-09-09T10:10:51Z","timestamp":1788948651000},"score":1,"resource":{"primary":{"URL":"https:\/\/academic.oup.com\/carcin\/article\/25\/11\/2089\/2475843"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[2004,11,1]]},"references-count":0,"journal-issue":{"issue":"11","published-print":{"date-parts":[[2004,11,1]]}},"URL":"https:\/\/doi.org\/10.1093\/carcin\/bgh227","relation":{},"ISSN":["1460-2180","0143-3334"],"issn-type":[{"value":"1460-2180","type":"electronic"},{"value":"0143-3334","type":"print"}],"subject":[],"published-other":{"date-parts":[[2004,11]]},"published":{"date-parts":[[2004,11,1]]}}}