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The 14-3-3\u03c3 isoform acts as a tumor suppressor and is often inactivated during tumor development.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Results<\/jats:title>\n            <jats:p>Here, we demonstrate enhanced CpG methylation of the 14-3-3\u03c3 gene in lymph node and cutaneous melanoma metastases compared with primary tumors, associated with dramatically reduced mRNA expression. In line with this, treatment of different metastatic melanoma cell lines with 5-aza-2'-deoxycytidine (5-Aza-CdR), a potent inhibitor of cytosine methylation, significantly induces 14-3-3\u03c3 protein expression. Additional treatment with histone deacetylase inhibitor 4-phenylbutyric acid (Pba) further enhances 14-3-3\u03c3 expression. Induction of 14-3-3\u03c3 expression by 5-Aza-CdR\/Pba treatment leads to almost complete inhibition of cell proliferation, with cells predominantly arrested in G2-M. The antiproliferative effect of 5-Aza-CdR\/Pba was reversed in 14-3-3\u03c3 knockdown cells. Similarly, melanoma cell lines stably overexpressing 14-3-3\u03c3 show dramatically reduced cell proliferation rates. Moreover, synchronous 14-3-3\u03c3 stably overexpressing cells do not progress through cell cycle, but display a permanent increase in the population of 4<jats:italic>n<\/jats:italic> DNA containing cells. Interestingly, overexpression of 14-3-3\u03c3 induces senescence of melanoma cells and is involved in melanoma cell senescence under genotoxic stress. Finally, 14-3-3\u03c3 knockdown supports migratory capacity of melanoma cells <jats:italic>in vitro<\/jats:italic>, while 14-3-3\u03c3 overexpression has opposing effects.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Conclusion<\/jats:title>\n            <jats:p>Taken together, the present report indicates that epigenetic silencing of 14-3-3\u03c3 might contribute to tumor progression in malignant melanoma via loss of cell cycle control, impaired cellular senescence program and support of migratory capacity.<\/jats:p>\n          <\/jats:sec>","DOI":"10.1186\/1476-4598-8-53","type":"journal-article","created":{"date-parts":[[2009,7,30]],"date-time":"2009-07-30T18:13:53Z","timestamp":1248977633000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":43,"title":["14-3-3\u03c3 gene silencing during melanoma progression and its role in cell cycle control and cellular senescence"],"prefix":"10.1186","volume":"8","author":[{"given":"Julia","family":"Schultz","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Saleh M","family":"Ibrahim","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Julio","family":"Vera","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Manfred","family":"Kunz","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"297","published-online":{"date-parts":[[2009,7,30]]},"reference":[{"key":"438_CR1","doi-asserted-by":"publisher","first-page":"51","DOI":"10.1056\/NEJMra052166","volume":"355","author":"AJ Miller","year":"2006","unstructured":"Miller AJ, Mihm MC: Melanoma. 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