Literature DB >> 30788686

H3K9me3, H3K36me3, and H4K20me3 Expression Correlates with Patient Outcome in Esophageal Squamous Cell Carcinoma as Epigenetic Markers.

Menghan Zhou1,2, Yiping Li3, Shaofeng Lin4,5, Yanping Chen6, Yanyan Qian1, Zhujiang Zhao1, Hong Fan7.   

Abstract

BACKGROUND: Histone methylation, as an essential pattern of posttranslational modifications, contributes to multiple cancer-related biological processes. Dysregulation of histone methylation is now considered a biomarker for cancer prognosis. AIMS: This study investigated and evaluated the potential role of four histone lysine trimethylation markers as biomarkers for esophageal squamous cell carcinoma (ESCC) prognosis.
METHODS: Tissue arrays were made from 135 paraffin-embedded ESCC samples and examined for histone markers by immunohistochemistry, and 10 pairs of cancer and noncancerous mucosa tissues from ESCC patients were investigated with Western blot. Chi-squared test, Kaplan-Meier analysis with log-rank test, and Cox proportional hazard trend analyses were performed to assess the prognostic values of the markers.
RESULTS: Histone 3 lysine 4 trimethylation (H3K4me3), histone 3 lysine 9 trimethylation (H3K9me3), and histone 4 lysine 20 trimethylation (H4K20me3), but not histone 3 lysine 36 trimethylation (H3K36me3), showed stronger immunostaining signals in tumor tissues than in the corresponding adjacent non-neoplastic mucosa tissues. The expression patterns of H3K36me3, H3K9me3, and H4K20me3 correlated with tumor infiltrating depth, lymph node involvement, and pTNM stage. Low-scoring H3K9me3 and H4K20me3 predicted better prognosis, while H3K36me3 manifested the opposite trend. Poor prognosis occurred in ESCC patients with expression patterns of high levels of H3K9me3, high levels of H4K20me3, and low levels of H3K36me3 expression.
CONCLUSIONS: H3K9me3, H4K20me3, and H3K36me3 showed a close relationship with clinical features and were considered independent risk factors for survival of ESCC patients. The combination of H3K9me3, H4K20me3, and H3K36me3 expression, rather than the expression of a single histone marker, is believed to further enhance evaluations of ESCC prognosis and management.

Entities:  

Keywords:  ESCC; Epigenetic marks; H3K36me3; H3K9me3; H4K20me3

Mesh:

Substances:

Year:  2019        PMID: 30788686     DOI: 10.1007/s10620-019-05529-2

Source DB:  PubMed          Journal:  Dig Dis Sci        ISSN: 0163-2116            Impact factor:   3.199


  55 in total

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Journal:  Cell       Date:  2005-11-18       Impact factor: 41.582

3.  Cross-talk between the H3K36me3 and H4K16ac histone epigenetic marks in DNA double-strand break repair.

Authors:  Lin Li; Yinsheng Wang
Journal:  J Biol Chem       Date:  2017-05-25       Impact factor: 5.157

4.  Increased H3K9me3 drives dedifferentiated phenotype via KLF6 repression in liposarcoma.

Authors:  Emily Z Keung; Kadir C Akdemir; Ghadah A Al Sannaa; Jeannine Garnett; Dina Lev; Keila E Torres; Alexander J Lazar; Kunal Rai; Lynda Chin
Journal:  J Clin Invest       Date:  2015-07-20       Impact factor: 14.808

5.  Broad H3K4me3 is associated with increased transcription elongation and enhancer activity at tumor-suppressor genes.

Authors:  Kaifu Chen; Zhong Chen; Dayong Wu; Lili Zhang; Xueqiu Lin; Jianzhong Su; Benjamin Rodriguez; Yuanxin Xi; Zheng Xia; Xi Chen; Xiaobing Shi; Qianben Wang; Wei Li
Journal:  Nat Genet       Date:  2015-08-24       Impact factor: 38.330

6.  Active genes are tri-methylated at K4 of histone H3.

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Journal:  Nature       Date:  2002-09-11       Impact factor: 49.962

Review 7.  Decoding the histone code: Role of H3K36me3 in mismatch repair and implications for cancer susceptibility and therapy.

Authors:  Guo-Min Li
Journal:  Cancer Res       Date:  2013-10-21       Impact factor: 12.701

Review 8.  Histone H4 lysine 20 methylation: key player in epigenetic regulation of genomic integrity.

Authors:  Stine Jørgensen; Gunnar Schotta; Claus Storgaard Sørensen
Journal:  Nucleic Acids Res       Date:  2013-01-23       Impact factor: 16.971

9.  Mapping H4K20me3 onto the chromatin landscape of senescent cells indicates a function in control of cell senescence and tumor suppression through preservation of genetic and epigenetic stability.

Authors:  David M Nelson; Farah Jaber-Hijazi; John J Cole; Neil A Robertson; Jeffrey S Pawlikowski; Kevin T Norris; Steven W Criscione; Nikolay A Pchelintsev; Desiree Piscitello; Nicholas Stong; Taranjit Singh Rai; Tony McBryan; Gabriel L Otte; Colin Nixon; William Clark; Harold Riethman; Hong Wu; Gunnar Schotta; Benjamin A Garcia; Nicola Neretti; Duncan M Baird; Shelley L Berger; Peter D Adams
Journal:  Genome Biol       Date:  2016-07-25       Impact factor: 13.583

10.  Inhibiting WEE1 Selectively Kills Histone H3K36me3-Deficient Cancers by dNTP Starvation.

Authors:  Sophia X Pfister; Enni Markkanen; Yanyan Jiang; Sovan Sarkar; Mick Woodcock; Giulia Orlando; Ioanna Mavrommati; Chen-Chun Pai; Lykourgos-Panagiotis Zalmas; Neele Drobnitzky; Grigory L Dianov; Clare Verrill; Valentine M Macaulay; Songmin Ying; Nicholas B La Thangue; Vincenzo D'Angiolella; Anderson J Ryan; Timothy C Humphrey
Journal:  Cancer Cell       Date:  2015-11-09       Impact factor: 31.743

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2.  Suv420 enrichment at the centromere limits Aurora B localization and function.

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Review 3.  H3K36 trimethylation-mediated biological functions in cancer.

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4.  Distinct histone H3 modification profiles correlate with aggressive characteristics of salivary gland neoplasms.

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5.  Comprehensive Analysis of Histone Modifications in Hepatocellular Carcinoma Reveals Different Subtypes and Key Prognostic Models.

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6.  Histone Mark Profiling in Pediatric Astrocytomas Reveals Prognostic Significance of H3K9 Trimethylation and Histone Methyltransferase SUV39H1.

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Review 7.  Clinicopathologic significance of protein lysine methyltransferases in cancer.

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