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Interaction between microRNA-181a and TNFAIP1 regulates pancreatic cancer proliferation and migration

Overview of attention for article published in Tumor Biology, July 2015
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Title
Interaction between microRNA-181a and TNFAIP1 regulates pancreatic cancer proliferation and migration
Published in
Tumor Biology, July 2015
DOI 10.1007/s13277-015-3704-8
Pubmed ID
Authors

Peng Zhang, Zhiyong Guo, Ronglin Hu, Xiaoshun He, Xingyuan Jiao, Xiaofeng Zhu

Abstract

We investigated the role of microRNA 181a (miR-181a) and its downstream target tumor necrosis factor, alpha-induced protein 1 (TNFAIP1) in pancreatic cancer regulation. Quantitative real-time PCR (qRT-PCR) was applied to evaluate the gene expression of miR-181a in seven pancreatic cancer cell lines. MiR-181a inhibitor lentivirus (miR-181a-IN) was used to down-regulate miR-181a in Capan-1 and AsPC-1 cells. The effects of miR-181a down-regulation on pancreatic cancer were evaluated by in vitro proliferation assay and migration assay. Targeting of miR-181a on TNFAIP1 in pancreatic cancer was evaluated by dual-luciferase reporter assay and western blot. TNFAIP1 was either upregulated by pcDNA3.1 (+) expression vector or down-regulated by siRNA in Capan-1 and AsPC-1 cells. The subsequent effects of TNFAIP1 upregulation or down-regulation on miR-181a mediated pancreatic cancer regulation were also evaluated through in vitro proliferation and migration assays. The in vivo effect of miR-181a down-regulation on pancreatic tumor growth was evaluated by a xenograft assay. MiR-181a was consistently upregulated in pancreatic cancer cell lines. MiR-181a down-regulation inhibited proliferation and migration in vitro, and upregulated TNFAIP1 in pancreatic cancer cells. Ectopic TNFAIP1 overexpression had similar tumor-suppressive effects on pancreatic cancer proliferation and migration as miR-181a down-regulation, whereas siRNA-mediated TNFAIP1 down-regulation had opposite or oncogenic effects on pancreatic cancer. In vivo pancreatic xenograft showed miR-181a recapitulated the in vitro anti-tumor effects and its regulation on TNFAIP1. MiR-181a played a critical role in regulating pancreatic cancer growth and migration, likely interacting with TNFAIP1.

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Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 10 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 10 100%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 2 20%
Researcher 2 20%
Professor 1 10%
Student > Master 1 10%
Other 1 10%
Other 0 0%
Unknown 3 30%
Readers by discipline Count As %
Medicine and Dentistry 2 20%
Immunology and Microbiology 1 10%
Biochemistry, Genetics and Molecular Biology 1 10%
Neuroscience 1 10%
Chemistry 1 10%
Other 0 0%
Unknown 4 40%
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 13 July 2015.
All research outputs
#20,282,766
of 22,816,807 outputs
Outputs from Tumor Biology
#1,834
of 2,622 outputs
Outputs of similar age
#218,971
of 262,361 outputs
Outputs of similar age from Tumor Biology
#113
of 170 outputs
Altmetric has tracked 22,816,807 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.
So far Altmetric has tracked 2,622 research outputs from this source. They receive a mean Attention Score of 2.2. 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 170 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.