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However, the effect of such an approach on survival of human melanoma cells remains less understood. Here, we show that the sphingosine analogue <jats:styled-content style=\"fixed-case\">FTY<\/jats:styled-content>720 that functionally antagonises S1<jats:styled-content style=\"fixed-case\">PR<\/jats:styled-content>s kills human melanoma cells through a mechanism involving the vacuolar H<jats:sup>+<\/jats:sup>\u2010<jats:styled-content style=\"fixed-case\">ATP<\/jats:styled-content>ase activity. Moreover, we demonstrate that <jats:styled-content style=\"fixed-case\">FTY<\/jats:styled-content>720\u2010triggered cell death is characterized by features of necrosis and is not dependent on receptor\u2010interacting protein kinase 1 or lysosome cathepsins, nor was it associated with the activation of protein phosphatase 2A. Instead, it is mediated by increased production of reactive oxygen species and is antagonized by activation of autophagy. Collectively, these results suggest that <jats:styled-content style=\"fixed-case\">FTY<\/jats:styled-content>720 and its analogues are promising candidates for further development as new therapeutic agents in the treatment of melanoma.<\/jats:p>","DOI":"10.1111\/pcmr.12326","type":"journal-article","created":{"date-parts":[[2014,10,31]],"date-time":"2014-10-31T04:44:37Z","timestamp":1414730677000},"page":"171-183","source":"Crossref","is-referenced-by-count":20,"title":["Involvement of vacuolar H<sup>+<\/sup>\u2010<scp>ATP<\/scp>ase in killing of human melanoma cells by the sphingosine kinase analogue <scp>FTY<\/scp>720"],"prefix":"10.1111","volume":"28","author":[{"given":"Kwang Hong","family":"Tay","sequence":"first","affiliation":[{"name":"School of Medicine and Public Health University of Newcastle Callaghan NSW Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xiaoying","family":"Liu","sequence":"additional","affiliation":[{"name":"School of Biomedical 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