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Expression of microRNA-96 and its potential functions by targeting FOXO3 in non-small cell lung cancer

Overview of attention for article published in Tumor Biology, October 2014
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Title
Expression of microRNA-96 and its potential functions by targeting FOXO3 in non-small cell lung cancer
Published in
Tumor Biology, October 2014
DOI 10.1007/s13277-014-2698-y
Pubmed ID
Authors

Juan Li, Ping Li, Tengfei Chen, Ge Gao, Xiaonan Chen, Yuwen Du, Ren Zhang, Rui Yang, Wei Zhao, Shaozhi Dun, Feng Gao, Guojun Zhang

Abstract

MicroRNAs are implicated in the regulation of various cellular processes, including proliferation, differentiation, cell death, and cell mobility, and can function either as oncogenes or tumor suppressors in tumor progression. The effects of the expression of miR-96 in non-small cell lung cancer (NSCLC) remain unclear. In our study, qRT-PCR (quantitative reverse transcription PCR) was performed to identify the miR-96 expression level in 68 paired NSCLC and adjacent normal lung tissues. Trans-well, cell counting kit-8, and apoptosis assays were used to evaluate the effects of miR-96 expression on cell invasion, proliferation, and apoptosis. Dual-luciferase reporter assay and Western blotting were used to verify whether FOXO3 was a potential major target gene of miR-96. Finally, the effect of FOXO3 on miR-96-induced cell survival was determined by transfection of the genes expressing FOXO3 lacking 3'UTR and miR-96. The expression level of miR-96 in NSCLC tissues was higher than that in adjacent normal lung tissues, and this increased expression was significantly associated with lymph node metastasis. In contrast to the cells in the blank and negative control groups, the number of cells migrating through the matrigel was significantly lower and the incidence of apoptosis was significantly higher in cells transfected with a miR-96 inhibitor. Western blotting and dual-luciferase reporter assays demonstrated that miR-96 can bind to the putative seed region in FOXO3 mRNA 3'UTR, and can significantly lower the expression of FOXO3. The introduction of FOXO3 cDNA without 3'UTR restored miR-96 induced cell apoptosis and invasion. MiR-96 is up-regulated in NSCLC tissues. Downregulation of miR-96 inhibits invasion and promotes apoptosis in NSCLC cells A549 and SPC-A-1 by targeting FOXO3. Therefore, our study improves our understanding of the mechanisms underlying NSCLC pathogenesis and may promote the development of novel targeted therapies.

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Mendeley readers

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 %
Student > Ph. D. Student 7 30%
Researcher 3 13%
Student > Bachelor 3 13%
Other 2 9%
Student > Doctoral Student 2 9%
Other 4 17%
Unknown 2 9%
Readers by discipline Count As %
Biochemistry, Genetics and Molecular Biology 7 30%
Medicine and Dentistry 6 26%
Agricultural and Biological Sciences 4 17%
Immunology and Microbiology 1 4%
Earth and Planetary Sciences 1 4%
Other 1 4%
Unknown 3 13%
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 October 2014.
All research outputs
#20,238,443
of 22,765,347 outputs
Outputs from Tumor Biology
#1,834
of 2,622 outputs
Outputs of similar age
#212,925
of 254,867 outputs
Outputs of similar age from Tumor Biology
#71
of 132 outputs
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