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miRNA-196b inhibits cell proliferation and induces apoptosis in HepG2 cells by targeting IGF2BP1

Overview of attention for article published in Molecular Cancer, April 2015
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  • Above-average Attention Score compared to outputs of the same age (55th percentile)

Mentioned by

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5 tweeters

Citations

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42 Dimensions

Readers on

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28 Mendeley
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Title
miRNA-196b inhibits cell proliferation and induces apoptosis in HepG2 cells by targeting IGF2BP1
Published in
Molecular Cancer, April 2015
DOI 10.1186/s12943-015-0349-6
Pubmed ID
Authors

Magali Rebucci, Audrey Sermeus, Elodie Leonard, Edouard Delaive, Marc Dieu, Maude Fransolet, Thierry Arnould, Carine Michiels

Abstract

Tumor hypoxia is one of the features of tumor microenvironment that contributes to chemoresistance. miRNAs have recently been shown to play important roles in tumorigenesis and drug resistance. Moreover, hypoxia also regulates the expression of a series of miRNAs. However, the interaction between chemoresistance, hypoxia and miRNAs has not been explored yet. The aim of this study is to understand the mechanisms activated/inhibited by miRNAs under hypoxia that induce resistance to chemotherapy-induced apoptosis. TaqMan low-density array was used to identify changes in miRNA expression when cells were exposed to etoposide under hypoxia or normoxia. The effects of miR-196b overexpression on apoptosis and cell proliferation were studied in HepG2 cells. miR-196b target mRNAs were identified by proteomic analysis, luciferase activity assay, RT-qPCR and western blot analysis. Results showed that hypoxia down-regulated miR-196b expression that was induced by etoposide. miR-196b overexpression increased the etoposide-induced apoptosis and reversed the protection of cell death observed under hypoxia. By a proteomic approach combined with bioinformatics analyses, we identified IGF2BP1 as a potential target of miR-196b. Indeed, miR-196b overexpression decreased IGF2BP1 RNA expression and protein level. The IGF2BP1 down-regulation by either miR-196b or IGF2BP1 siRNA led to an increase in apoptosis and a decrease in cell viability and proliferation in normal culture conditions. However, IGF2BP1 silencing did not modify the chemoresistance induced by hypoxia, probably because it is not the only target of miR-196b involved in the regulation of apoptosis. In conclusion, for the first time, we identified IGF2BP1 as a direct and functional target of miR-196b and showed that miR-196b overexpression reverses the chemoresistance induced by hypoxia. These results emphasize that the chemoresistance induced by hypoxia is a complex mechanism.

Twitter Demographics

The data shown below were collected from the profiles of 5 tweeters who shared this research output. Click here to find out more about how the information was compiled.

Mendeley readers

The data shown below were compiled from readership statistics for 28 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
India 1 4%
Brazil 1 4%
Unknown 26 93%

Demographic breakdown

Readers by professional status Count As %
Researcher 8 29%
Student > Bachelor 4 14%
Student > Ph. D. Student 4 14%
Student > Master 3 11%
Other 2 7%
Other 4 14%
Unknown 3 11%
Readers by discipline Count As %
Agricultural and Biological Sciences 9 32%
Biochemistry, Genetics and Molecular Biology 6 21%
Medicine and Dentistry 4 14%
Earth and Planetary Sciences 2 7%
Environmental Science 1 4%
Other 0 0%
Unknown 6 21%

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 15 January 2016.
All research outputs
#10,989,575
of 19,211,930 outputs
Outputs from Molecular Cancer
#618
of 1,456 outputs
Outputs of similar age
#108,290
of 244,041 outputs
Outputs of similar age from Molecular Cancer
#1
of 1 outputs
Altmetric has tracked 19,211,930 research outputs across all sources so far. This one is in the 42nd percentile – i.e., 42% of other outputs scored the same or lower than it.
So far Altmetric has tracked 1,456 research outputs from this source. They receive a mean Attention Score of 4.2. This one has gotten more attention than average, scoring higher than 57% 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 244,041 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 55% of its contemporaries.
We're also able to compare this research output to 1 others from the same source and published within six weeks on either side of this one. This one has scored higher than all of them