Genome-wide analysis of H3K36me3 and its regulations to cancer-related genes expression in human cell lines

Zhang, Lu-Qiang; Li, Qian‐Zhong; Jin, Wen; Zuo, Yongchun; Guo, Sheng

doi:10.1016/j.biosystems.2018.07.004

Cited by 14 publications

(15 citation statements)

References 51 publications

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“…Previous studies and our findings have reported that the changes in HM signals play key roles in gene expression changes ( Zhang et al, 2011 , 2018 ; Liu et al, 2013 ; Zhang and Li, 2017 , 2020 ). To investigate the impacts of each HM in different bins on gene expression changes, we first identify the DEGs between normal and CML cells.…”

Section: Resultssupporting

confidence: 59%

“…Not surprisingly, the broad roles of H3K79me2 and H3K36me3 make them increasingly important in treating developmental defects and diseases. Besides that, our previous studies ( Zhang and Li, 2017 , 2020 ; Zhang et al, 2018 ) demonstrate that 86.2% of expressed sequence tags are enriched in gene body regions. Of these tags in the gene body regions, 90.8% of tags are distributed in intron regions.…”

Section: Discussionmentioning

confidence: 75%

“…Recent investigators have revealed that the pathogenesis of CML is closely related to the dynamic changes of HMs ( Zhang and Li, 2017 , 2020 ; Zhang et al, 2017 , 2018 ). In this research, according to Eq.…”

Section: Resultsmentioning

confidence: 99%

“…Studies have revealed that the pathogenesis of CML is associated with the activation of oncogenes and inactivation of tumor suppressor genes. The loss-of-function mutations of these CML-related genes are linked to the dynamic alterations of histone modifications (HMs) ( Zhang and Li, 2017 , 2020 ; Zhang et al, 2017 , 2018 ). As an integral part of HMs, histone acetylation and methylation are the most investigated modifications that are reversible, and the aberrations of HMs and the mutations of their modulators are associated with leukemogenesis ( Zhang et al, 2004 ; Funata et al, 2017 ).…”

Section: Introductionmentioning

confidence: 99%

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Identification of Key Histone Modifications and Their Regulatory Regions on Gene Expression Level Changes in Chronic Myelogenous Leukemia

Zhang

Fan

Liu

et al. 2021

Front. Cell Dev. Biol.

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Chronic myelogenous leukemia (CML) is a type of cancer with a series of characteristics that make it particularly suitable for observations on leukemogenesis. Research have exhibited that the occurrence and progression of CML are associated with the dynamic alterations of histone modification (HM) patterns. In this study, we analyze the distribution patterns of 11 HM signals and calculate the signal changes of these HMs in CML cell lines as compared with that in normal cell lines. Meanwhile, the impacts of HM signal changes on expression level changes of CML-related genes are investigated. Based on the alterations of HM signals between CML and normal cell lines, the up- and down-regulated genes are predicted by the random forest algorithm to identify the key HMs and their regulatory regions. Research show that H3K79me2, H3K36me3, and H3K27ac are key HMs to expression level changes of CML-related genes in leukemogenesis. Especially H3K79me2 and H3K36me3 perform their important functions in all 100 bins studied. Our research reveals that H3K79me2 and H3K36me3 may be the core HMs for the clinical treatment of CML.

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Section: Resultssupporting

confidence: 59%

Section: Discussionmentioning

confidence: 75%

Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Identification of Key Histone Modifications and Their Regulatory Regions on Gene Expression Level Changes in Chronic Myelogenous Leukemia

Zhang

Fan

Liu

et al. 2021

Front. Cell Dev. Biol.

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“…H3K36me3 was shown to have the highest degree of epigenetic modification hubs that were altered by NO exposure. H3K36me3 was also found to be associated with a poor prognosis in hepatocellular carcinoma (60) and corelated with cancer-related gene expression in cancer cell lines (61). In addition, H3K79Me3 is one of the histone modifications of interest due to controlling epithelial-to-mesenchymal (EMT) (62) and the stemness of certain cells (63).…”

Section: Discussionmentioning

confidence: 99%

Microarray-based Analysis of Genes, Transcription Factors, and Epigenetic Modifications in Lung Cancer Exposed to Nitric Oxide

Maiuthed

Prakhongcheep

Chanvorachote

2020

Cancer Genomics Proteomics

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Background/Aim: Nitric oxide (NO) is recognized as an important biological mediator that exerts several human physiological functions. As its nature is an aqueous soluble gas that can diffuse through cells and tissues, NO can affect cell signaling, the phenotype of cancer and modify surrounding cells. The variety of effects of NO on cancer cell biology has convinced researchers to determine the defined mechanisms of these effects and how to control this mediator for a better understanding as well as for therapeutic gain. Materials and Methods: We used bioinformatics and pharmacological experiments to elucidate the potential regulation and underlying mechanisms of NO in non-small a lung cancer cell model. Results: Using microarrays, we identified a total of 151 NO-regulated genes (80 upregulated genes, 71 down-regulated genes) with a strong statistically significant difference compared to untreated controls. Among these, the genes activated by a factor of more than five times were: DCBLD2,

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EGFR transcription in non‐small‐cell lung cancer tumours can be revealed in ctDNA by cell‐free chromatin immunoprecipitation (cfChIP)

et al. 2021

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Determination of tumour-specific transcription based on liquid biopsies possesses a large diagnostic and prognostic potential in non-small cell lung cancer (NSCLC). Cell-free DNA (cfDNA) packed in nucleosomes mirrors the histone modification profiles present in the cells of origin. H3 lysine 36 trimethylation (H3K36me3)-modified nucleosomes are associated with active genes and, therefore, cell-free chromatin immunoprecipitation (cfChIP) of H3K36me3-associated cfDNA has the potential to delineate whether transcription of a particular gene is occurring in the cells from which its cfDNA originates. We hypothesized that cfChIP can delineate transcriptional status of genes harbouring somatic cancer mutations and analysed the recurrently observed EGFR-L858R mutation as an example. In representative NSCLC cell lines, the relationship between wild type (WT) and mutated EGFR transcriptional activity and mRNA expression levels was analysed using H3K36me3 ChIP and EGFR mRNA reverse transcription quantitative PCR (RT-qPCR), respectively. The ChIP analysis showed that both WT and mutated EGFR are transcribed, and that mRNA is similarly expressed per EGFR copy. Based on this observation, we proceeded with EGFR cfChIP using blood plasma from NSCLC patients harbouring the EGFR-L858R mutation. EGFR-WT fragments can originate from both non-tumour cells with no or low EGFR transcription and tumour cells with active EGFR transcription, whereas EGFR-L858R fragments must specifically originate from tumour cells. H3K36me3 cfChIP followed by droplet digital PCR (ddPCR) revealed significantly higher enrichment of EGFR-L858R compared to EGFR-WT fragments. This is in alignment with EGFR-L858R being actively transcribed in the NSCLC tumour cells. This study is proof-ofprinciple that cfChIP can be used to identify tumour-specific transcriptional activity of mutated alleles, which can expand the utility of liquid-biopsy-based cfDNA analyses to enhance tumour diagnostics and therapeutics.

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Genome-wide analysis of H3K36me3 and its regulations to cancer-related genes expression in human cell lines

Cited by 14 publications

References 51 publications

Identification of Key Histone Modifications and Their Regulatory Regions on Gene Expression Level Changes in Chronic Myelogenous Leukemia

Identification of Key Histone Modifications and Their Regulatory Regions on Gene Expression Level Changes in Chronic Myelogenous Leukemia

Microarray-based Analysis of Genes, Transcription Factors, and Epigenetic Modifications in Lung Cancer Exposed to Nitric Oxide

EGFR transcription in non‐small‐cell lung cancer tumours can be revealed in ctDNA by cell‐free chromatin immunoprecipitation (cfChIP)

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