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Previous studies showed that the proapoptotic effects of GD3 can be counteracted by 9\u2010O\u2010acetylation. To determine whether 9\u2010O\u2010acetyl GD3 (acGD3) has a general antiapoptotic potential, the apoptosis\u2010sensitive Jurkat cell line and an apoptosis\u2010sensitive variant of the cell line Molt\u20104 were preincubated with micromolar concentrations of acGD3 and then treated with inducers of apoptosis. A reduced apoptotic index and an increased cell viability were observed. On the other hand, when the Jurkat cells were treated with GD3 for extended periods of time, a population was selected that was resistant to apoptosis induction by <jats:italic>N<\/jats:italic>\u2010acetyl sphingosine as well as by the anti\u2010leukemic drug daunorubicin. Comparative analysis of gangliosides revealed the formation of acGD3 in the resistant Jurkat cells that was not found in the apoptosis\u2010sensitive cells. Conversely, exposing the acGD3 positive and apoptosis\u2010resistant cell line Molt\u20104 to the O\u2010deacetylating activity of salicylate resulted in a complete disappearance of acGD3 and an enhanced sensitivity to <jats:italic>N<\/jats:italic>\u2010acetyl sphingosine\u2010mediated apoptosis. Formation of acGD3 might thus represent a new mechanism how tumor cells can escape apoptosis. \u00a9 2006 Wiley\u2010Liss, Inc.<\/jats:p>","DOI":"10.1002\/ijc.21788","type":"journal-article","created":{"date-parts":[[2006,1,23]],"date-time":"2006-01-23T18:16:47Z","timestamp":1138040207000},"page":"67-73","source":"Crossref","is-referenced-by-count":59,"title":["9\u2010O\u2010acetyl GD3 protects tumor cells from 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