Qihong Li1, Haiyan Sun1, Yao Shu1, Xuan Zou1, Yantao Zhao2, Cheng Ge1. 1. Department of Stomatology, Affiliated Hospital of Academy of Military Medical Sciences, Beijing, 100071, China. 2. Department of Orthopaedics, First Affiliated Hospital of the General Hospital of People's Liberation Army, Beijing, 100048, China.
Abstract
OBJECTIVES: MOF (males absent on the first) is a histone acetyltransferase belonging to the MYST (MOZ, Ybf2/Sas3, Sas2 and TIP60) family. In mammals, MOF plays critical roles in transcription activation by acetylating histone H4 at K16. Human MOF (hMOF) essentially participates in behaviour of several human cancers. However, its role in human oral tongue squamous cell carcinoma (OTSCC) remains elusive, but we propose that hMOF regulates OTSCC cell population growth. MATERIALS AND METHODS: Real time PCR and western blot analysis were applied, and it was found that hMOF level was up-regulated in human OTSCC. High hMOF expression predicted poor overall and disease-free survival. hMOF knockdown attenuated OTSCC cell growth and transformation. RESULTS: EZH2 (enhancer of zeste homolog 2) was up-regulated in human OTSCC tissues and its level positively correlated with level of hMOF. hMOF knockdown inhibited EZH2 expression by reducing its promoter activity. Moreover, we have demonstrated that EZH2 was critically essential for function of hMOF in human OTSCC. CONCLUSIONS: Human males absent on the first regulated OSTCC growth through EZH2, thus EZH2 may serve as a candidate for anti-OTSCC therapy.
OBJECTIVES: MOF (males absent on the first) is a histone acetyltransferase belonging to the MYST (MOZ, Ybf2/Sas3, Sas2 and TIP60) family. In mammals, MOF plays critical roles in transcription activation by acetylating histone H4 at K16. Human MOF (hMOF) essentially participates in behaviour of several human cancers. However, its role in human oral tongue squamous cell carcinoma (OTSCC) remains elusive, but we propose that hMOF regulates OTSCC cell population growth. MATERIALS AND METHODS: Real time PCR and western blot analysis were applied, and it was found that hMOF level was up-regulated in human OTSCC. High hMOF expression predicted poor overall and disease-free survival. hMOF knockdown attenuated OTSCC cell growth and transformation. RESULTS: EZH2 (enhancer of zeste homolog 2) was up-regulated in human OTSCC tissues and its level positively correlated with level of hMOF. hMOF knockdown inhibited EZH2 expression by reducing its promoter activity. Moreover, we have demonstrated that EZH2 was critically essential for function of hMOF in human OTSCC. CONCLUSIONS: Human males absent on the first regulated OSTCC growth through EZH2, thus EZH2 may serve as a candidate for anti-OTSCC therapy.
Authors: Daria G Valerio; Haiming Xu; Chun-Wei Chen; Takayuki Hoshii; Meghan E Eisold; Christopher Delaney; Monica Cusan; Aniruddha J Deshpande; Chun-Hao Huang; Amaia Lujambio; YuJun George Zheng; Johannes Zuber; Tej K Pandita; Scott W Lowe; Scott A Armstrong Journal: Cancer Res Date: 2017-02-15 Impact factor: 12.701