Objective To elucidate the role of ΔNp63α in its regulation of manganese superoxide dismutase (SOD2) and suppression of apoptosis. Methods Human non-transformed mammary epithelial Michigan Cancer Foundation-10 A (MCF-10 A) cells tably expressing ΔNp63α were subjected to quantitative polymerase chain reaction (Q-PCR) and Western blot analyses as well as apoptosis assays for SOD2 and, under the condition of suspension growth of MCF-10 A cells. Results Overexpression of ΔNp63α transcriptionally activated SOD2 expression, resulting in reduced reactive oxygen species (ROS) levels and decreasing apoptosis under the condition of suspension growth of MCF-10 A. Conclusions ΔNp63α activates transcription of SOD2 and is concomitant with reduced apoptosis, suggesting a role for SOD2 in ΔNp63α-mediated tumorigenesis.%目的 研究p53家族成员ΔNp63α转录激活锰超氧化物歧化酶 (SOD2) 在细胞凋亡中的抑制作用.方法 在人永生化乳腺上皮细胞MCF-10A中过表达ΔNp63α,检测SOD2 mRNA和蛋白水平的变化情况;在悬浮条件下检测过表达ΔNp63α的MCF-10A细胞中SOD2、活性氧小分子 (ROS) 和细胞凋亡的变化情况.结果 在人永生化乳腺上皮细胞MCF-10A中过表达ΔNp63α后可以转录激活SOD2;ΔNp63α通过转录激活SOD2来清除ROS进而抑制细胞凋亡.结论 ΔNp63α通过转录激活SOD2并抑制细胞凋亡,提示这可能是其参与肿瘤发生的机制之一.
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