HELLS Regulates Chromatin Remodeling and Epigenetic Silencing of Multiple Tumor Suppressor Genes in Human Hepatocellular Carcinoma

Hepatology ◽  
2019 ◽  
Vol 69 (5) ◽  
pp. 2013-2030 ◽  
Author(s):  
Cheuk‐Ting Law ◽  
Lai Wei ◽  
Felice Ho‐Ching Tsang ◽  
Cerise Yuen‐Ki Chan ◽  
Iris Ming‐Jing Xu ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Tumor Suppressor ◽  
Chromatin Remodeling ◽  
Tumor Suppressor Genes ◽  
Human Hepatocellular Carcinoma ◽  
Epigenetic Silencing ◽  
Suppressor Genes ◽  
Multiple Tumor

Loss of heterozygosity and methylation of multiple tumor suppressor genes on chromosome 3 in hepatocellular carcinoma

2012 ◽  
Vol 48 (1) ◽  
pp. 132-143 ◽  
Author(s):  
Xiaoying Zhang ◽  
Hiu Ming Li ◽  
Zhiyan Liu ◽  
Gengyin Zhou ◽  
Qinghui Zhang ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Tumor Suppressor ◽  
Loss Of Heterozygosity ◽  
Tumor Suppressor Genes ◽  
Chromosome 3 ◽  
Suppressor Genes ◽  
Multiple Tumor

scholarly journals Aberrant methylation of multiple tumor suppressor genes in aging liver, chronic hepatitis, and hepatocellular carcinoma

Hepatology ◽  
2007 ◽  
Vol 47 (3) ◽  
pp. 908-918 ◽  
Author(s):  
Naoshi Nishida ◽  
Takeshi Nagasaka ◽  
Takafumi Nishimura ◽  
Iwao Ikai ◽  
C. Richard Boland ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Chronic Hepatitis ◽  
Tumor Suppressor ◽  
Tumor Suppressor Genes ◽  
Aberrant Methylation ◽  
Suppressor Genes ◽  
Multiple Tumor

scholarly journals Modification of Epigenetic Histone Acetylation in Hepatocellular Carcinoma

Cancers ◽  
2018 ◽  
Vol 10 (1) ◽  
pp. 8 ◽  
Author(s):  
Kwei-Yan Liu ◽  
Li-Ting Wang ◽  
Shih-Hsien Hsu
Keyword(s):  
Hepatocellular Carcinoma ◽  
Tumor Suppressor ◽  
Tumor Suppressor Genes ◽  
Chemical Sensor ◽  
Enzyme Level ◽  
Tumor Therapy ◽  
Tumor Formation ◽  
Current Evidence ◽  
Epigenetic Changes ◽  
Suppressor Genes

Cells respond to various environmental factors such as nutrients, food intake, and drugs or toxins by undergoing dynamic epigenetic changes. An imbalance in dynamic epigenetic changes is one of the major causes of disease, oncogenic activities, and immunosuppressive effects. The aryl hydrocarbon receptor (AHR) is a unique cellular chemical sensor present in most organs, and its dysregulation has been demonstrated in multiple stages of tumor progression in humans and experimental models; however, the effects of the pathogenic mechanisms of AHR on epigenetic regulation remain unclear. Apart from proto-oncogene activation, epigenetic repressions of tumor suppressor genes are involved in tumor initiation, procession, and metastasis. Reverse epigenetic repression of the tumor suppressor genes by epigenetic enzyme activity inhibition and epigenetic enzyme level manipulation is a potential path for tumor therapy. Current evidence and our recent work on deacetylation of histones on tumor-suppressive genes suggest that histone deacetylase (HDAC) is involved in tumor formation and progression, and treating hepatocellular carcinoma with HDAC inhibitors can, at least partially, repress tumor proliferation and transformation by recusing the expression of tumor-suppressive genes such as TP53 and RB1.

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