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Upregulation of microRNA-122 by farnesoid X receptor suppresses the growth of hepatocellular carcinoma cells

Overview of attention for article published in Molecular Cancer, August 2015
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  • Above-average Attention Score compared to outputs of the same age (56th percentile)
  • Good Attention Score compared to outputs of the same age and source (71st percentile)

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Title
Upregulation of microRNA-122 by farnesoid X receptor suppresses the growth of hepatocellular carcinoma cells
Published in
Molecular Cancer, August 2015
DOI 10.1186/s12943-015-0427-9
Pubmed ID
Authors

Jialin He, Kai Zhao, Lu Zheng, Zhizhen Xu, Wei Gong, Shan Chen, Xiaodong Shen, Gang Huang, Min Gao, Yijun Zeng, Yan Zhang, Fengtian He

Abstract

microRNA-122 (miR-122) is the most abundant and specific miRNA in the liver. It acts as an important tumor suppressor in hepatocellular carcinoma (HCC) through regulating its target genes, but details of its own regulation are largely unknown. Farnesoid X receptor (FXR), a transcription factor with multiple functions, plays an important role in protecting against liver carcinogenesis, but it is unclear whether the anti-HCC effect of FXR is involved in the regulation of miR-122. The levels of miR-122 and FXR in HCC tissues and cell lines were examined by quantitative real-time PCR (qRT-PCR). qRT-PCR was also used to detect the expression of miR-122 target genes at mRNA level, while Western blotting was used to analyze that of their protein products. The effect of FXR on the transcriptional activity of miR-122 promoter was evaluated by a luciferase reporter assay. Electrophoretic mobility shift assay (EMSA) and chromatin immunoprecipitation (ChIP) assay were performed to identify the FXR binding site within miR-122 promoter region. The cell proliferation was analyzed by a CCK-8 assay. The influence of FXR on tumor growth and miR-122 expression in vivo was monitored using HCC xenografts in nude mice. The expression of FXR was positively correlated with that of miR-122 in HCC tissues and cell lines. Activation of FXR in HCC cells upregulated miR-122 expression and in turn downregulated the expression of miR-122 target genes including insulin-like growth factor-1 receptor and cyclin G1. FXR bound directly to the DR2 element (-338 to -325) in miR-122 promoter region, and enhanced the promoter's transcriptional activity. Functional experiments showed that the FXR-mediated upregulation of miR-122 suppressed the proliferation of HCC cells in vitro and the growth of HCC xenografts in vivo. miR-122 is a novel target gene of FXR, and the upregulation of miR-122 by FXR represses the growth of HCC cells, suggesting that FXR may serve as a key transcriptional regulator for manipulating miR-122 expression, and the FXR/miR-122 pathway may therefore be a novel target for the treatment of HCC.

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X Demographics

The data shown below were collected from the profiles of 4 X users who shared this research output. Click here to find out more about how the information was compiled.
Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 22 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 22 100%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 4 18%
Researcher 4 18%
Student > Master 4 18%
Other 2 9%
Student > Doctoral Student 1 5%
Other 3 14%
Unknown 4 18%
Readers by discipline Count As %
Agricultural and Biological Sciences 7 32%
Biochemistry, Genetics and Molecular Biology 4 18%
Immunology and Microbiology 3 14%
Medicine and Dentistry 2 9%
Chemistry 1 5%
Other 0 0%
Unknown 5 23%
Attention Score in Context

Attention Score in Context

This research output has an Altmetric Attention Score of 3. 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 04 January 2016.
All research outputs
#12,740,022
of 22,824,164 outputs
Outputs from Molecular Cancer
#775
of 1,721 outputs
Outputs of similar age
#115,832
of 267,539 outputs
Outputs of similar age from Molecular Cancer
#12
of 45 outputs
Altmetric has tracked 22,824,164 research outputs across all sources so far. This one is in the 43rd percentile – i.e., 43% of other outputs scored the same or lower than it.
So far Altmetric has tracked 1,721 research outputs from this source. They typically receive a little more attention than average, with a mean Attention Score of 5.7. This one has gotten more attention than average, scoring higher than 54% of its peers.
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 267,539 tracked outputs that were published within six weeks on either side of this one in any source. This one has gotten more attention than average, scoring higher than 56% of its contemporaries.
We're also able to compare this research output to 45 others from the same source and published within six weeks on either side of this one. This one has gotten more attention than average, scoring higher than 71% of its contemporaries.