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MicroRNA-505 functions as a tumor suppressor in endometrial cancer by targeting TGF-α

Overview of attention for article published in Molecular Cancer, February 2016
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Title
MicroRNA-505 functions as a tumor suppressor in endometrial cancer by targeting TGF-α
Published in
Molecular Cancer, February 2016
DOI 10.1186/s12943-016-0496-4
Pubmed ID
Authors

Shuo Chen, Kai-Xuan Sun, Bo-Liang Liu, Zhi-Hong Zong, Yang Zhao

Abstract

Endometrial carcinoma (EC) is one of the most lethal gynecologic cancers. Patients frequently have regional or distant metastasis at diagnosis. MicroRNAs are small non-coding RNAs that participate in numerous biological processes. Recent studies have demonstrated that miR-505 is associated with several types of cancer; however, the expression and function of miR-505 have not been investigated in EC. miR-505 expression in normal endometrial tissue, endometrial carcinomas were quantified by Quantitative reverse transcription PCR. The endometrial carcinoma cell lines HEC-1B and Ishikawa were each transfected with miR-505 or scrambled mimics, after which cell phenotype and expression of relevant molecules were assayed. Dual-luciferase reporter assay and a xenograft mouse model were used to examine miR-505 and its target gene TGF-α. RT-PCR results demonstrated that miR-505 was significantly downregulated in human EC tissues compared to normal endometrial tissues. Besides, miR-505 expression was negatively associated with FIGO stage (stage I-II vs. III-IV), and lymph node metastasis (negative vs. positive). In vitro, overexpression of miR-505 significantly suppressed EC cell proliferation, increased apoptosis and reduced migratory and invasive activity. A miR-505 binding site was identified in the 3' untranslated region of TGF-α mRNA (TGFA) using miRNA target-detecting software; a dual luciferase reporter assay confirmed that miR-505 directly targets and regulates TGFA. RT-PCR and Western-blotting results indicated that overexpressing miR-505 reduced the expression of TGF-α and the TGF-α-regulated proteins MMP2, MMP9, CDK2, while induced Bax and cleaved-PARP expression in EC cells. In vivo, overexpression of miR-505 reduced the tumorigenicity and inhibited the growth of xenograft tumors in a mouse model of EC. Taken together, this study demonstrates that miR-505 acts as tumor suppressor in EC by regulating TGF-α.

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Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 40 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 40 100%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 8 20%
Student > Master 7 18%
Student > Bachelor 5 13%
Researcher 5 13%
Other 2 5%
Other 1 3%
Unknown 12 30%
Readers by discipline Count As %
Biochemistry, Genetics and Molecular Biology 12 30%
Agricultural and Biological Sciences 9 23%
Medicine and Dentistry 3 8%
Pharmacology, Toxicology and Pharmaceutical Science 1 3%
Engineering 1 3%
Other 0 0%
Unknown 14 35%
Attention Score in Context

Attention Score in Context

This research output has an Altmetric Attention Score of 2. 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 02 September 2016.
All research outputs
#13,964,379
of 22,842,950 outputs
Outputs from Molecular Cancer
#866
of 1,721 outputs
Outputs of similar age
#201,683
of 397,125 outputs
Outputs of similar age from Molecular Cancer
#9
of 25 outputs
Altmetric has tracked 22,842,950 research outputs across all sources so far. This one is in the 37th percentile – i.e., 37% of other outputs scored the same or lower than it.
So far Altmetric has tracked 1,721 research outputs from this source. They typically receive a little more attention than average, with a mean Attention Score of 5.7. This one is in the 47th percentile – i.e., 47% of its peers scored the same or lower than it.
Older research outputs will score higher simply because they've had more time to accumulate mentions. To account for age we can compare this Altmetric Attention Score to the 397,125 tracked outputs that were published within six weeks on either side of this one in any source. This one is in the 47th percentile – i.e., 47% of its contemporaries scored the same or lower than it.
We're also able to compare this research output to 25 others from the same source and published within six weeks on either side of this one. This one has gotten more attention than average, scoring higher than 64% of its contemporaries.