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组蛋白乙酰转移酶 hMOF 促进肺癌细胞进入 S 期并促进肿瘤发生。

Histone acetyltransferase hMOF promotes S phase entry and tumorigenesis in lung cancer.

机构信息

Institute of Epigenetics and Cancer Research, School of Medicine, Tsinghua University, Medical Science Building C-315, Beijing 100084, China.

出版信息

Cell Signal. 2013 Aug;25(8):1689-98. doi: 10.1016/j.cellsig.2013.04.006. Epub 2013 Apr 28.

DOI:10.1016/j.cellsig.2013.04.006
PMID:23628702
Abstract

hMOF is the major acetyltransferase of histone H4 lysine 16 (H4K16) in humans, but its biological function is not well understood. In this study, hMOF was found to be more frequently highly expressed in non-small cell lung cancer (NSCLC) than corresponding normal tissues (P < 0.001). In addition, up-regulation of H4K16 acetylation was also more frequent in NSCLC than normal tissues (P = 0.002). Furthermore, hMOF promotes the cell proliferation, migration and adhesion of NSCLC cell lines. Microarray analysis and chromatin immunoprecipitation (ChIP) assays suggest that hMOF modulates proliferation and metastasis by regulating histone H4K16 acetylation at the promoter regions of downstream target genes. Moreover, hMOF promotes S phase entry via Skp2. These findings suggest that hMOF contributes to NSCLC tumorigenesis.

摘要

hMOF 是人类组蛋白 H4 赖氨酸 16(H4K16)的主要乙酰转移酶,但它的生物学功能尚不清楚。在这项研究中,与相应的正常组织相比,hMOF 在非小细胞肺癌(NSCLC)中表达更高(P<0.001)。此外,在 NSCLC 中,H4K16 乙酰化的上调也比正常组织更频繁(P=0.002)。此外,hMOF 促进 NSCLC 细胞系的细胞增殖、迁移和黏附。微阵列分析和染色质免疫沉淀(ChIP)实验表明,hMOF 通过调节下游靶基因启动子区域的组蛋白 H4K16 乙酰化来调节增殖和转移。此外,hMOF 通过 Skp2 促进 S 期进入。这些发现表明 hMOF 有助于 NSCLC 的肿瘤发生。

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