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本文引用的文献

1
Reduced abundance of the E3 ubiquitin ligase E6AP contributes to decreased expression of the INK4/ARF locus in non-small cell lung cancer.E3泛素连接酶E6AP丰度降低导致非小细胞肺癌中INK4/ARF基因座表达下降。
Sci Signal. 2017 Jan 10;10(461):eaaf8223. doi: 10.1126/scisignal.aaf8223.
2
Hypermethylated DNA as a biomarker for colorectal cancer: a systematic review.DNA高甲基化作为结直肠癌的生物标志物：一项系统综述。
Colorectal Dis. 2016 Jun;18(6):549-61. doi: 10.1111/codi.13336.
3
MOZ (MYST3, KAT6A) inhibits senescence via the INK4A-ARF pathway.MOZ（MYST3，KAT6A）通过 INK4A-ARF 通路抑制衰老。
Oncogene. 2015 Nov 19;34(47):5807-20. doi: 10.1038/onc.2015.33. Epub 2015 Mar 16.
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Combination epigenetic therapy has efficacy in patients with refractory advanced non-small cell lung cancer.联合表观遗传学治疗对难治性晚期非小细胞肺癌患者有效。
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An efficient high-throughput screening method for MYST family acetyltransferases, a new class of epigenetic drug targets.一种针对MYST家族乙酰转移酶的高效高通量筛选方法，MYST家族乙酰转移酶是一类新型表观遗传药物靶点。
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E6AP is required for replicative and oncogene-induced senescence in mouse embryo fibroblasts.E6AP 对于小鼠胚胎成纤维细胞的复制和癌基因诱导的衰老过程是必需的。
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7
Ink4a/Arf and oncogene-induced senescence prevent tumor progression during alternative colorectal tumorigenesis.INK4a/ARF 和癌基因诱导的衰老可防止结直肠肿瘤发生的替代途径中的肿瘤进展。
Cancer Cell. 2010 Aug 9;18(2):135-46. doi: 10.1016/j.ccr.2010.06.013.
8
Core signaling pathways in human pancreatic cancers revealed by global genomic analyses.通过全基因组分析揭示的人类胰腺癌核心信号通路。
Science. 2008 Sep 26;321(5897):1801-6. doi: 10.1126/science.1164368. Epub 2008 Sep 4.
9
Inhibition of DNA methylation and histone deacetylation prevents murine lung cancer.抑制DNA甲基化和组蛋白去乙酰化可预防小鼠肺癌。
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10
INK4a-deficient human diploid fibroblasts are resistant to RAS-induced senescence.INK4a基因缺陷的人二倍体成纤维细胞对RAS诱导的衰老具有抗性。
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揭示p16基因沉默的新途径：对肺癌的治疗意义

Uncovering a novel pathway for p16 silencing: Therapeutic implications for lung cancer.

作者信息

Gamell C, Gulati T, Solomon B, Haupt S, Haupt Y

机构信息

The Sir Peter MacCallum Department of Oncology, The University of Melbourne, Melbourne, VIC, Australia.

Tumor Suppression Laboratory, Peter MacCallum Cancer Centre, Melbourne, VIC, Australia.

出版信息

Mol Cell Oncol. 2017 Mar 7;4(5):e1299273. doi: 10.1080/23723556.2017.1299273. eCollection 2017.

DOI:10.1080/23723556.2017.1299273
PMID:29057301
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5644485/
Abstract

A key step during onset of most cases of non-small cell lung cancer (NSCLC) is the loss of the tumor suppressor p16 (best known as p16), commonly due to promoter hypermethylation. We recently reported a novel regulatory pathway involving E6-associated protein and cell division control protein 6, which provides a methylation-independent mechanism for p16 silencing in patients with a particularly aggressive form of NSCLC.

摘要

在大多数非小细胞肺癌（NSCLC）病例发病过程中的一个关键步骤是肿瘤抑制因子p16（最为人所知的是p16）的缺失，这通常是由于启动子高甲基化所致。我们最近报道了一条涉及E6相关蛋白和细胞分裂控制蛋白6的新型调控途径，该途径为一种特别侵袭性形式的NSCLC患者的p16沉默提供了一种不依赖甲基化的机制。