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Notch1信号通路在调节细胞的增殖、分化和凋亡中起重要作用。Notch1信号通路的异常激活可促进乳腺癌的发生、发展,但调控此过程的表观遗传机制尚有待于阐明。本研究发现,与相应的癌旁组织相比,乳腺癌组织中Notch1活性片段NIC1呈高表达,而组蛋白H4第16位赖氨酸残基乙酰化(H4K16ac)水平较低。敲低MCF-7细胞中Notch1可导致H4K16ac水平升高,且MCF-7细胞的增殖和迁移能力下降。本研究结果提示表观遗传修饰H4K16ac参与乳腺癌细胞Notch1致瘤信号传递,为乳腺癌发生、发展的机制研究提供了新思路。
Notch1 signaling plays an important role in regulating cell proliferation, differentiation and apoptosis. The abnormal activation of Notch1 signaling pathway can promote the occurrence and development of breast cancer, but the epigenetic mechanism regulating this process remains to be elucidated. This study found that, compared with the corresponding paracancerous tissue, Notch1 activity in the breast cancer tissue NIC1 was highly expressed, while the histone H4 16 lysine residue acetylation (H4K16ac) level is low. Knockdown of Notchl in MCF-7 cells resulted in an increase in H4K16ac levels and a decrease in the ability of MCF-7 cells to proliferate and migrate. Our results suggest that epigenetic modification of H4K16ac is involved in the tumorigenic signaling of breast cancer cells Notch1, which provides a new idea for the study of the mechanism of breast cancer.