NASP antagonize chromatin accessibility through maintaining histone H3K9me1 in hepatocellular carcinoma

Kang, Xuan; Feng, Yun; Gan, Zhixue; Zeng, Shiyang; Guo, Xinying; Chen, Xirui; Zhang, Ye; Wang, Chen; Liu, Kui-nan; Chen, Xuelin; Jiang, Xiaoxue; Song, Shuting; Li, Yabin; Chen, Su; Sun, Feng; Mao, Zhiyong; Yang, Xiaomei; Chang, Jian-Feng

doi:10.1016/j.bbadis.2018.07.033

Cited by 17 publications

(14 citation statements)

References 47 publications

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“…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). H3K9Me1 has exhibited capacity for liver cancer formation (64) and was found to be a prognosis marker in oral cancer and oropharyngeal squamous cell carcinoma (65).…”

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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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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“…It is expressed in all cells undergoing division. Functions of NASP mainly involve liver cancer [54], immune response [55], and cell proliferation [56]. For example, previous studies have shown that in lupus model mice, NASP gene mutation can change the proportion of immune cells in the spleen and aggravate the autoimmune response [55].…”

Section: Discussionmentioning

confidence: 99%

Associations between gut microbiota and hand grip strength: a polygenetic scoring analysis and genome-wide environmental interaction study

Liu¹,

Cheng²,

Wen³

et al. 2020

Preprint

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Background We aim to explore the genetic association between hand grip strength (HGS) and gut microbiota (GM). Methods The genome-wide association study (GWAS) data of GM was obtained from a recently published study, involving 2,646 individuals. Phenotypic data of left HGS (n = 375,229) and right HGS (n = 375,279) were derived from the UK Biobank. Firstly, PLINK 2.0 was used to calculate 114 GM related polygenetic risk score (PRS) of each subject based on GWAS result. Regression analysis was then conducted to evaluate the possible association of GM-PRS and HGS. Then genome-wide by environment interaction study (GWEIS) of GM related traits was then performed using a regression model adjusted for age, gender, BMI and 10 principal components. Results For PRS analysis, 13 candidate GM were identified to be associated with left HGS (P < 0.05), including G_Bifidobacterium (P = 8.36 × 10− 4), G_Clostridium_sensu_stricto (P = 2.69 × 10− 3), and 10 significant GM for right HGS, such as G_Acidaminococcus (P = 1.29 × 10− 2), G_Streptococcus (P = 1.79 × 10− 2). In addition, 4 GM were found to be overlapped in association with both left and right HGS, including G_Bifidobacterium (P right HGS = 2.78 × 10− 2, P left HGS = 8.36 × 10− 4). Furthermore, several genome-wide significant GWEIS associations were detected for HGS, including 3 significant SNPs interacted with G_Butyricicoccus (P < 5 × 10− 8) for right HGS (rs41310432, P = 3.86 × 10− 8; closest gene: NASP; rs1053941, P = 4.71 × 10− 8; closest gene: NASP; rs6671239, P = 4.73 × 10− 8, closest gene: GPBP1L1), and 1 suggestive intronic SNP in CACNA1H on chromosome 16 interacted with G_Butyricicoccus (rs139206507, P = 8.68 × 10− 8 ) for left HGS. Conclusions Our study holds great potential gaining a better understanding of the relationship between GM and HGS.

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“…The levels of H3K9me2/me3 have been found to be enriched in nongenic regions, which resulted in heterochromatin formation and epigenetic silencing, while H3K9me1 levels were enriched at active genes and open chromatin [38, 39]. Moreover, histone demethylation and chromatin decondensation can lead to dysregulated gene expression and transcriptional activation of gene targets [8, 27, 40].…”

Section: Discussionmentioning

confidence: 99%

KDM3B suppresses APL progression by restricting chromatin accessibility and facilitating the ATRA-mediated degradation of PML/RARα

Wang

Fan

et al. 2019

Cancer Cell Int

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Background A hallmark of acute promyelocytic leukemia (APL) is the expression of PML/RARα fusion protein. Treatment with all-trans retinoic acid (ATRA) results in the terminal differentiation of neutrophil granulocytes. However, the underlying mechanisms remain largely unknown. Here, we identify and elucidate a novel differentiation-suppressive model of APL involving the histone demethylase KDM3B, which has been identified as a suppressor of the tumor genes involved in hematopoietic malignancies. Methods First, we established a KDM3B knockdown NB4 cell model to determine the functional characteristics of KDM3B by cell proliferation assay and flow cytometry. Then, we performed ChIP-seq and ATAC-seq to search for potential relationships among KDM3B, histone modification (H3K9me1/me2) and the chromatin state. Finally, molecular biological techniques and a multi-omics analysis were used to explore the role of KDM3B in differentiation of the leukemia cells after ATRA treatment. Results We found that knocking down KDM3B contributed to the growth of NB4 APL cells via the promotion of cell-cycle progression and blocked granulocytic differentiation. Through global and molecular approaches, we provided futher evidence that knocking down KDM3B altered the global distribution of H3K9me1/me2 and increased the chromatin accessibility. Moreover, knocking down KDM3B inhibited the ATRA-induced degradation of the PML/RARα oncoprotein. Conclusion Our study suggested that KDM3B was able to inhibit APL progression by maintaining chromatin in a compact state and facilitating the ATRA-mediated degradation of PML/RARα. Taken together, the results show that KDM3B may be an alternative target for the treatment regimens and the targeted therapy for APL by sustaining the function of PML/RARα fusion protein.

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NASP antagonize chromatin accessibility through maintaining histone H3K9me1 in hepatocellular carcinoma

Cited by 17 publications

References 47 publications

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

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

Associations between gut microbiota and hand grip strength: a polygenetic scoring analysis and genome-wide environmental interaction study

KDM3B suppresses APL progression by restricting chromatin accessibility and facilitating the ATRA-mediated degradation of PML/RARα

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