Cell Death Dis:西达本胺通过表观遗传修饰抑制细胞自噬发挥抗骨髓瘤活性

2020-05-20 QQY MedSci原创

细胞自噬过程会导致异常的细胞质组分出现自噬小体依赖性的溶酶体降解反应,其涉及了一系列以如LC3B1-3在内的自噬相关(ATG)蛋白为核心组成的细胞膜动态重塑过程。

细胞自噬过程会导致异常的细胞质组分出现自噬小体依赖性的溶酶体降解反应,其涉及了一系列以如LC3B1-3在内的自噬相关(ATG)蛋白为核心组成的细胞膜动态重塑过程。

近期研究发现,细胞的自噬诱导与表观遗传学染色质改变息息相关,尤其是组蛋白H4第16位赖氨酸的乙酰化(H4K16ac)以及组蛋白H3第27位赖氨酸的三甲基化(H3K27me3)修饰。组蛋白修饰酶(hMOF、SIRT1和EZH2)已被证实是细胞自噬反应的关键调节因子。

多发性骨髓瘤(MM)是一种浆细胞恶性肿瘤。在多发性骨髓瘤中,抑制细胞自噬和泛素蛋白酶体降解这两种截然不同的协同蛋白水解途径是一种潜在的有希望的治疗策略。

西达本胺(Chidamide)是一种新型的苯甲酰胺类的组蛋白脱乙酰基酶抑制剂,具有较强的抗骨髓瘤活性。

在该研究中,研究人员发现,西达本胺在骨髓瘤细胞中具有抑制细胞自噬的作用。研究人员发现,西达本胺治疗能够显著下调组蛋白脱乙酰基酶SIRT1的表达水平,同时会导致乙酰转移酶hMOF和组蛋白甲基转移酶EZH2的表达水平出现剂量依赖性的上调,最终导致H4K16ac和H3K27me3的整体水平升高。

进一步的实验发现,在自噬相关基因LC3B的启动子区域中,H4K16ac和H3K27me3的水平同时上调,从而增强了这两种修饰在西达本胺介导的LC3B转录抑制中的特定作用。

最后,实验结果显示西达本胺和蛋白酶体抑制剂硼替佐米(bortezomib)的共同治疗表现出针对MM细胞的显著的协同细胞毒性,这与泛素化蛋白积累的增加、过度的内质网应激反应以及失调的未折叠蛋白反应相关。

以上研究结果表明,西达本胺能够部分通过表观遗传修饰抑制泛素化蛋白相关的细胞自噬降解,并与硼替佐米协同增强抗骨髓瘤活性。

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    2020-05-22 cy0328
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    2020-05-22 zhangyxzsh

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