DNA damage induced activation of Cygb stabilizes p53 and mediates G1 arrest

摘要: Cytoglobin (Cygb) is an emerging tumor suppressor gene silenced by promoter hypermethylation in many human tumors. So far, the precise molecular mechanism underlying its suppressive function remains poorly understood. Here, we identified Cygb as a genotoxic stress-responsive hemoprotein upregulated upon sensing cellular DNA damage. Our studies demonstrated that physically associates with and stabilizes p53, key damage signaling factor. We provide evidence extends half-life of p53 blocking ubiquitination subsequent degradation. show that, damage, cells overexpressing displayed proliferation defect rapid accumulation target p21, while knockdown failed to efficiently arrest G1 phase response insult. These results suggest possible involvement mediating thereby contributing maintenance genomic integrity. study thus presents novel insight into mechanistic role suppression.