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In mammals, <jats:styled-content style=\"fixed-case\">MOF<\/jats:styled-content> plays critical roles in transcription activation by acetylating histone H4 at K16. Human MOF (<jats:styled-content style=\"fixed-case\">hMOF<\/jats:styled-content>) essentially participates in behaviour of several human cancers. However, its role in human oral tongue squamous cell carcinoma (<jats:styled-content style=\"fixed-case\">OTSCC<\/jats:styled-content>) remains elusive, but we propose that <jats:styled-content style=\"fixed-case\">hMOF<\/jats:styled-content> regulates <jats:styled-content style=\"fixed-case\">OTSCC<\/jats:styled-content> cell population growth.<\/jats:p><\/jats:sec><jats:sec><jats:title>Materials and methods<\/jats:title><jats:p>Real time <jats:styled-content style=\"fixed-case\">PCR<\/jats:styled-content> and western blot analysis were applied, and it was found that <jats:italic><jats:styled-content style=\"fixed-case\">hMOF<\/jats:styled-content><\/jats:italic> level was up\u2010regulated in human <jats:styled-content style=\"fixed-case\">OTSCC<\/jats:styled-content>. High <jats:italic><jats:styled-content style=\"fixed-case\">hMOF<\/jats:styled-content><\/jats:italic> expression predicted poor overall and disease\u2010free survival. <jats:italic><jats:styled-content style=\"fixed-case\">hMOF<\/jats:styled-content><\/jats:italic> knockdown attenuated <jats:styled-content style=\"fixed-case\">OTSCC<\/jats:styled-content> cell growth and transformation.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p><jats:italic>EZH2<\/jats:italic> (enhancer of zeste homolog 2) was up\u2010regulated in human <jats:styled-content style=\"fixed-case\">OTSCC<\/jats:styled-content> tissues and its level positively correlated with level of <jats:italic><jats:styled-content style=\"fixed-case\">hMOF<\/jats:styled-content><\/jats:italic>. <jats:italic><jats:styled-content style=\"fixed-case\">hMOF<\/jats:styled-content><\/jats:italic> knockdown inhibited <jats:italic><jats:styled-content style=\"fixed-case\">EZH2<\/jats:styled-content><\/jats:italic> expression by reducing its promoter activity. Moreover, we have demonstrated that <jats:italic><jats:styled-content style=\"fixed-case\">EZH2<\/jats:styled-content><\/jats:italic> was critically essential for function of <jats:styled-content style=\"fixed-case\">hMOF<\/jats:styled-content> in human <jats:styled-content style=\"fixed-case\">OTSCC<\/jats:styled-content>.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>Human males absent on the first regulated <jats:styled-content style=\"fixed-case\">OSTCC<\/jats:styled-content> growth through <jats:italic><jats:styled-content style=\"fixed-case\">EZH2<\/jats:styled-content><\/jats:italic>, thus <jats:italic><jats:styled-content style=\"fixed-case\">EZH2<\/jats:styled-content><\/jats:italic> may serve as a candidate for anti\u2010<jats:styled-content style=\"fixed-case\">OTSCC<\/jats:styled-content> 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