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miR-200c Inhibits invasion, migration and proliferation of bladder cancer cells through down-regulation of BMI-1 and E2F3

Overview of attention for article published in Journal of Translational Medicine, November 2014
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Title
miR-200c Inhibits invasion, migration and proliferation of bladder cancer cells through down-regulation of BMI-1 and E2F3
Published in
Journal of Translational Medicine, November 2014
DOI 10.1186/s12967-014-0305-z
Pubmed ID
Authors

Lei Liu, Mingning Qiu, Guobin Tan, Ziji Liang, Yue Qin, Lieqian Chen, Hege Chen, Jianjun Liu

Abstract

BackgroundMicroRNA-200c (miR-200c) is one of the short noncoding RNAs that play crucial roles in tumorigenesis and tumor progression. It also acts as considerable modulator in the process of epithelial-to-mesenchymal transition (EMT), a cell development regulating process that affects tumor development and metastasis. However, the role of miR-200c in bladder cancer cells and its mechanism has not been well studied. The purpose of this study was to determine the potential role of miR-200c in regulating EMT and how it contributed to bladder cancer cells in invasion, migration and proliferation.MethodsReal-time reverse transcription-PCR was used to identify and validate the differential expression of MiR-200c involved in EMT in 4 bladder cancer cell lines and clinical specimens. A list of potential miR-200 direct targets was identified through the TargetScan database. The precursor of miR-200c was over-expressed in UMUC-3 and T24 cells using a lentivirus construct, respectively. Protein expression and signaling pathway modulation were validated through Western blot analysis and confocal microscopy, whereas BMI-1 and E2F3, direct target of miR-200c, were validated by using the wild-type and mutant 3¿-untranslated region BMI-1/E2F3 luciferase reporters.ResultsWe demonstrate that MiR-200c is down-regulated in bladder cancer specimens compared with adjacent ones in the same patient. Luciferase assays showed that the direct down-regulation of BMI-1 and E2F3 were miR-200c-dependent because mutations in the two putative miR-200c-binding sites have rescued the inhibitory effect. Over-expression of miR-200c in bladder cancer cells resulted in significantly decreased the capacities of cell invasion, migration and proliferation. miR-200c over-expression resulted in conspicuous down-regulation of BMI-1and E2F3 expression and in a concomitant increase in E-cadherin levels.ConclusionsmiR-200c appears to control the EMT process through BMI-1 in bladder cancer cells, and it inhibits their proliferation through down-regulating E2F3. The targets of miR-200c include BMI-1 and E2F3, which are a novel regulator of EMT and a regulator of proliferation, respectively.

Twitter Demographics

The data shown below were collected from the profile of 1 tweeter 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 29 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Germany 1 3%
Unknown 28 97%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 9 31%
Student > Doctoral Student 5 17%
Other 3 10%
Student > Bachelor 3 10%
Student > Master 2 7%
Other 5 17%
Unknown 2 7%
Readers by discipline Count As %
Biochemistry, Genetics and Molecular Biology 7 24%
Agricultural and Biological Sciences 4 14%
Medicine and Dentistry 3 10%
Pharmacology, Toxicology and Pharmaceutical Science 2 7%
Nursing and Health Professions 1 3%
Other 6 21%
Unknown 6 21%

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 05 November 2014.
All research outputs
#18,968,277
of 21,321,610 outputs
Outputs from Journal of Translational Medicine
#3,063
of 3,686 outputs
Outputs of similar age
#212,620
of 253,680 outputs
Outputs of similar age from Journal of Translational Medicine
#204
of 285 outputs
Altmetric has tracked 21,321,610 research outputs across all sources so far. This one is in the 1st percentile – i.e., 1% of other outputs scored the same or lower than it.
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We're also able to compare this research output to 285 others from the same source and published within six weeks on either side of this one. This one is in the 1st percentile – i.e., 1% of its contemporaries scored the same or lower than it.