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MicroRNA-26a suppresses epithelial-mesenchymal transition in human hepatocellular carcinoma by repressing enhancer of zeste homolog 2

Overview of attention for article published in Journal of Hematology & Oncology, January 2016
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Title
MicroRNA-26a suppresses epithelial-mesenchymal transition in human hepatocellular carcinoma by repressing enhancer of zeste homolog 2
Published in
Journal of Hematology & Oncology, January 2016
DOI 10.1186/s13045-015-0229-y
Pubmed ID
Authors

De-Ning Ma, Zong-Tao Chai, Xiao-Dong Zhu, Ning Zhang, Di-Hua Zhan, Bo-Gen Ye, Cheng-Hao Wang, Cheng-Dong Qin, Yi-Ming Zhao, Wei-Ping Zhu, Man-Qing Cao, Dong-Mei Gao, Hui-Chuan Sun, Zhao-You Tang

Abstract

Our previous study reported that microRNA-26a (miR-26a) inhibited tumor progression by inhibiting tumor angiogenesis and intratumoral macrophage infiltration in hepatocellular carcinoma (HCC). The direct roles of miR-26a on tumor cell invasion remain poorly understood. In this study, we aim to explore the mechanism of miR-26a in modulating epithelial-mesenchymal transition (EMT) in HCC. In vitro cell morphology and cell migration were compared between the hepatoma cell lines HCCLM3 and HepG2, which were established in the previous study. Overexpression and down-regulation of miR-26a were induced in these cell lines, and Western blot and immunofluorescence assays were used to detect the expression of EMT markers. Xenograft nude mouse models were used to observe tumor growth and pulmonary metastasis. Immunohistochemical assays were conducted to study the relationships between miR-26a expression and enhancer of zeste homolog 2 (EZH2) and E-cadherin expression in human HCC samples. Down-regulation of miR-26a in HCCLM3 and HepG2 cells resulted in an EMT-like cell morphology and high motility in vitro and increased in tumor growth and pulmonary metastasis in vivo. Through down-regulation of EZH2 expression and up-regulation of E-cadherin expression, miR-26a inhibited the EMT process in vitro and in vivo. Luciferase reporter assay showed that miR-26a directly interacted with EZH2 messenger RNA (mRNA). Furthermore, the expression of miR-26a was positively correlated with E-cadherin expression and inversely correlated with EZH2 expression in human HCC tissue. miR-26a inhibited the EMT process in HCC by down-regulating EZH2 expression.

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Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 27 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 27 100%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 6 22%
Student > Master 4 15%
Student > Postgraduate 4 15%
Researcher 3 11%
Other 2 7%
Other 3 11%
Unknown 5 19%
Readers by discipline Count As %
Biochemistry, Genetics and Molecular Biology 9 33%
Agricultural and Biological Sciences 5 19%
Immunology and Microbiology 2 7%
Medicine and Dentistry 2 7%
Chemistry 1 4%
Other 1 4%
Unknown 7 26%
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 08 January 2016.
All research outputs
#17,780,575
of 22,837,982 outputs
Outputs from Journal of Hematology & Oncology
#869
of 1,192 outputs
Outputs of similar age
#267,482
of 393,663 outputs
Outputs of similar age from Journal of Hematology & Oncology
#6
of 12 outputs
Altmetric has tracked 22,837,982 research outputs across all sources so far. This one is in the 19th percentile – i.e., 19% of other outputs scored the same or lower than it.
So far Altmetric has tracked 1,192 research outputs from this source. They typically receive more attention than average, with a mean Attention Score of 9.7. This one is in the 22nd percentile – i.e., 22% 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 393,663 tracked outputs that were published within six weeks on either side of this one in any source. This one is in the 27th percentile – i.e., 27% of its contemporaries scored the same or lower than it.
We're also able to compare this research output to 12 others from the same source and published within six weeks on either side of this one. This one is in the 41st percentile – i.e., 41% of its contemporaries scored the same or lower than it.