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miR-508-3p concordantly silences NFKB1 and RELA to inactivate canonical NF-κB signaling in gastric carcinogenesis

Overview of attention for article published in Molecular Cancer, January 2016
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Title
miR-508-3p concordantly silences NFKB1 and RELA to inactivate canonical NF-κB signaling in gastric carcinogenesis
Published in
Molecular Cancer, January 2016
DOI 10.1186/s12943-016-0493-7
Pubmed ID
Authors

Tingting Huang, Wei Kang, Bin Zhang, Feng Wu, Yujuan Dong, Joanna H. M. Tong, Weiqin Yang, Yuhang Zhou, Li Zhang, Alfred S. L. Cheng, Jun Yu, Ka Fai To

Abstract

NF-κB signaling pathway plays an important role in gastric carcinogenesis. The basic expression and functional role of NFKB1 and RELA (components of canonical NF-κB pathway) in gastric cancer (GC) have not been well elucidated. In this study, the role of NFKB1 and RELA in gastric tumorigenesis will be investigated and their regulation by microRNAs (miRNAs) will be deeply explored. The mRNA and protein expression of NFKB1 and RELA were investigated by qRT-PCR and Western blot in GC cell lines and primary tumors. The functional roles of NFKB1 and RELA in GC were demonstrated by MTT proliferation assay, monolayer colony formation, cell invasion and migration, cell cycle analysis and in vivo study through siRNA mediated knockdown. Identification of NFKB1 as a direct target of tumor suppressor miRNA miR-508-3p was achieved by expression regulation assays together with dual luciferase activity experiments. NFKB1 and RELA were up-regulated in GC cell lines and primary tumors compared with normal gastric epithelium cells and their upregulation correlation with poor survival in GC. siRNA mediated knockdown of NFKB1 or RELA exhibited anti-oncogenic effect both in vitro and in vivo. NFKB1 was further revealed to be a direct target of miR-508-3p in gastric tumorigenesis and their expression showed negative correlation in primary GC samples. miR-508-3p was down-regulated in GC cells compared with normal gastric epithelium samples and its ectopic expression in GC cell lines also exerts tumor suppressor function. NFKB1 re-expression was found to partly abolish the tumor-suppressive effect of miR-508-3p in GC. All these findings supports that canonical NF-κB signaling pathway is activated in GC at least by the inactivation of miR-508-3p and this might have therapeutic potential in GC treatment.

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Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 36 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 36 100%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 8 22%
Student > Master 7 19%
Researcher 4 11%
Student > Bachelor 2 6%
Professor 2 6%
Other 5 14%
Unknown 8 22%
Readers by discipline Count As %
Biochemistry, Genetics and Molecular Biology 11 31%
Medicine and Dentistry 6 17%
Agricultural and Biological Sciences 3 8%
Unspecified 1 3%
Environmental Science 1 3%
Other 2 6%
Unknown 12 33%
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 24 January 2016.
All research outputs
#18,436,183
of 22,840,638 outputs
Outputs from Molecular Cancer
#1,291
of 1,721 outputs
Outputs of similar age
#285,815
of 395,188 outputs
Outputs of similar age from Molecular Cancer
#21
of 30 outputs
Altmetric has tracked 22,840,638 research outputs across all sources so far. This one is in the 11th percentile – i.e., 11% of other outputs scored the same or lower than it.
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