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Upregulation of microRNA-96 and its oncogenic functions by targeting CDKN1A in bladder cancer

Overview of attention for article published in Cancer Cell International, November 2015
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Title
Upregulation of microRNA-96 and its oncogenic functions by targeting CDKN1A in bladder cancer
Published in
Cancer Cell International, November 2015
DOI 10.1186/s12935-015-0235-8
Pubmed ID
Authors

Ziyu Wu, Kun Liu, Yunyan Wang, Zongyuan Xu, Junsong Meng, Shuo Gu

Abstract

Genome-wide miRNA expression profile has identified microRNA (miR)-96 as one of upregulated miRNAs in clinical bladder cancer (BC) tissues compared to normal bladder tissues. The aim of this study was to confirm the expression pattern of miR-96 in BC tissues and to investigate its involvement in carcinogenesis. Quantitative real-time PCR was performed to detect the expression levels of miR-96 in 60 BC and 40 normal control tissues. Bioinformatics prediction combined with luciferase reporter assay were used to verify whether the cyclin-dependent kinase inhibitor CDKN1A was a potential target gene of miR-96. Cell counting kit-8 and apoptosis assays were further performed to evaluate the effects of miR-96-CDKN1A axis on cell proliferation and apoptosis of BC cell lines. We validated that miR-96 was significantly increased in both human BC tissues and cell lines. According to the data of miRTarBase, CDKN1A might be a candidate target gene of miR-96. In addition, luciferase reporter and Western blot assays respectively demonstrated that miR-96 could bind to the putative seed region in CDKN1A mRNA 3'UTR, and significantly reduce the expression level of CDKN1A protein. Moreover, we found that the inhibition of miR-96 expression remarkably decreased cell proliferation and promoted cell apoptosis of BC cell lines, which was consistent with the findings observed following the introduction of CDKN1A cDNA without 3'UTR restored miR-96. Our data reveal that miR-96 may function as an onco-miRNA in BC. Upregulation of miR-96 may contribute to aggressive malignancy partly through suppressing CDKN1A protein expression in BC cells.

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 23 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 23 100%

Demographic breakdown

Readers by professional status Count As %
Researcher 5 22%
Student > Bachelor 4 17%
Student > Postgraduate 3 13%
Unspecified 3 13%
Student > Doctoral Student 3 13%
Other 5 22%
Readers by discipline Count As %
Biochemistry, Genetics and Molecular Biology 7 30%
Medicine and Dentistry 6 26%
Unspecified 5 22%
Agricultural and Biological Sciences 4 17%
Earth and Planetary Sciences 1 4%
Other 0 0%

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 20 November 2015.
All research outputs
#5,620,772
of 6,588,247 outputs
Outputs from Cancer Cell International
#227
of 286 outputs
Outputs of similar age
#196,434
of 248,210 outputs
Outputs of similar age from Cancer Cell International
#25
of 40 outputs
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So far Altmetric has tracked 286 research outputs from this source. They receive a mean Attention Score of 3.6. This one is in the 1st percentile – i.e., 1% of its peers scored the same or lower than it.
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We're also able to compare this research output to 40 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.