Targeting EZH2 regulates tumor growth and apoptosis through modulating mitochondria dependent cell-death pathway in HNSCC
Copyright policy )Targeting EZH2 regulates tumor growth and apoptosis through modulating mitochondria dependent cell-death pathway in HNSCC
EZH2 is a negative prognostic factor and is overexpressed or activated in most human cancers including head and neck squamous cell carcinoma (HNSCC). Analysis of The Cancer Genome Atlas (TCGA) HNSCC data indicated that EZH2 over-expression was associated with high tumor grade and conferred poor prognosis. EZH2 inhibition triggered cell apoptosis, cell cycle arrest and decreased cell growth in vitro. MICU1 (mitochondrial calcium uptake1) was shown to be down regulated when EZH2 expression was inhibited in HNSCC. When the EZH2 and MICU1 were inhibited, HNSCC cells became susceptible to cell cycle arrest and apoptosis. Mitochondrial membrane potential and cytosolic Ca2+ concentration analysis suggested that EZH2 and MICU1 were required to maintain mitochondrial membrane potential stability. A xenograft tumor model was used to confirm that EZH2 depletion inhibited HNSCC cell growth and induced tumor cell apoptosis. In summary, EZH2 is a potential anti-tumor target in HNSCC.
- University of Oklahoma United States
- University of Oklahoma Health Sciences Center United States
- Dartmouth College United States
- Tianjin Medical University General Hospital China (People's Republic of)
- Tianjin Medical University Cancer Institute and Hospital China (People's Republic of)
Male, Mice, Inbred BALB C, Squamous Cell Carcinoma of Head and Neck, Polycomb Repressive Complex 2, Mice, Nude, Apoptosis, Middle Aged, Survival Analysis, Mitochondria, Mice, Head and Neck Neoplasms, Cell Line, Tumor, Carcinoma, Squamous Cell, Animals, Humans, Enhancer of Zeste Homolog 2 Protein, Female, Cell Proliferation
Male, Mice, Inbred BALB C, Squamous Cell Carcinoma of Head and Neck, Polycomb Repressive Complex 2, Mice, Nude, Apoptosis, Middle Aged, Survival Analysis, Mitochondria, Mice, Head and Neck Neoplasms, Cell Line, Tumor, Carcinoma, Squamous Cell, Animals, Humans, Enhancer of Zeste Homolog 2 Protein, Female, Cell Proliferation
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