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EZH2 promotes hepatocellular carcinoma progression through modulating miR-22/galectin-9 axis

Overview of attention for article published in Journal of Experimental & Clinical Cancer Research, January 2018
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Title
EZH2 promotes hepatocellular carcinoma progression through modulating miR-22/galectin-9 axis
Published in
Journal of Experimental & Clinical Cancer Research, January 2018
DOI 10.1186/s13046-017-0670-6
Pubmed ID
Authors

Shaofei Chen, Jiarui Pu, Jie Bai, Yuping Yin, Ke Wu, Jiliang Wang, Xiaoming Shuai, Jinbo Gao, Kaixiong Tao, Guobin Wang, Hang Li

Abstract

Recent studies have shown that interferon-γ (IFN-γ)-induced galectin-9 expression in Kupffer cells plays an essential role in modulatingthe microenvironment of hepatitis-associated hepatocellular carcinoma (HCC). However, whether or not IFN-γ induces galectin-9 expression in HCC cells, its biological role and regulatory mechanism in HCC development and progression are poorly defined. Quantitative PCR and western blotting analysis were used to detect galectin-9 and EZH2 levels in HCC cell lines stimulated with IFN-γ. Bioinformatics analysis and luciferase reporter assay were utilized to confirmthe binding ofmiR-22 to the 3' untranslated region (3'-UTR) of galectin-9. The methylation status of miR-22 promoter was analyzed by MSP (Methylation specific PCR) and BSP (bisulfite sequencing PCR), while chromatin immunoprecipitation (ChIP) assay identify the occupation status of EZH2 and H3K27me3 at the promoter. Furthermore, the effect of ectopic expression of galectin-9 and miR-22 on cell proliferation, migration, invasion and cell apoptosis was assessed by using CCK-8, transwell assays and flow cytometric analysis, respectively. IFN-γ induces up-regulation of galectin-9 and EZH2 in HCC cell lines. Galectin-9 is a target of miR-22 and EZH2 facilitates galectin-9 expression by tri-methylation of H3K27 on miR-22 promoter but not hyper-methylation status of DNA. MiR-22 overexpression suppressed HCC cell growth, invasion, and metastasis both in vitro and in vivo. Interestingly, galectin-9 also exhibited antitumor effects, and restoring galectin-9 expression in miR-22 overexpressing cells strengthened its antitumor effects. These findings indicated that EZH2 facilitates galectin-9 expression by epigenetically repressing miR-22 and that galectin-9, which is known as an immunosuppressant, also functions as a tumor suppressor in HCC.

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Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 26 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 26 100%

Demographic breakdown

Readers by professional status Count As %
Student > Master 4 15%
Student > Bachelor 3 12%
Researcher 3 12%
Student > Ph. D. Student 3 12%
Student > Postgraduate 2 8%
Other 3 12%
Unknown 8 31%
Readers by discipline Count As %
Biochemistry, Genetics and Molecular Biology 5 19%
Medicine and Dentistry 5 19%
Unspecified 1 4%
Veterinary Science and Veterinary Medicine 1 4%
Immunology and Microbiology 1 4%
Other 3 12%
Unknown 10 38%
Attention Score in Context

Attention Score in Context

This research output has an Altmetric Attention Score of 1. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 12 January 2018.
All research outputs
#20,663,600
of 25,382,440 outputs
Outputs from Journal of Experimental & Clinical Cancer Research
#1,636
of 2,380 outputs
Outputs of similar age
#344,794
of 450,867 outputs
Outputs of similar age from Journal of Experimental & Clinical Cancer Research
#27
of 43 outputs
Altmetric has tracked 25,382,440 research outputs across all sources so far. This one is in the 10th percentile – i.e., 10% of other outputs scored the same or lower than it.
So far Altmetric has tracked 2,380 research outputs from this source. They receive a mean Attention Score of 4.8. This one is in the 17th percentile – i.e., 17% of its peers scored the same or lower than it.
Older research outputs will score higher simply because they've had more time to accumulate mentions. To account for age we can compare this Altmetric Attention Score to the 450,867 tracked outputs that were published within six weeks on either side of this one in any source. This one is in the 13th percentile – i.e., 13% of its contemporaries scored the same or lower than it.
We're also able to compare this research output to 43 others from the same source and published within six weeks on either side of this one. This one is in the 27th percentile – i.e., 27% of its contemporaries scored the same or lower than it.