Evidence map›Paper›PMID 26337669›Full record

ArticleCell death and differentiation2016

Downregulation of microRNA-362-3p and microRNA-329 promotes tumor progression in human breast cancer.

H Kang, C Kim, H Lee, J G Rho, J-W Seo, J-W Nam, W K Song, S W Nam, W Kim, E K Lee

Open access · bronzeAbstract read
In one paragraph

Article in Cell death and differentiation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
3.0field-weighted citation impact, top 8% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

49 citing papers in PubMed, 103 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors at 4 institutions in 1 country.

H KangDepartment of Biochemistry, College of Medicine, The Catholic University of Korea, Seoul, South Korea.
C KimDepartment of Biochemistry, College of Medicine, The Catholic University of Korea, Seoul, South Korea.
H LeeDepartment of Biochemistry, College of Medicine, The Catholic University of Korea, Seoul, South Korea.
J G RhoDepartment of Molecular Science and Technology, Ajou University, Suwon, South Korea.
J-W SeoDepartment of Life Science, College of Natural Sciences, Hanyang University, Seoul, South Korea.
J-W NamDepartment of Life Science, College of Natural Sciences, Hanyang University, Seoul, South Korea.
W K SongDepartment of Life Science, Bio Imaging and Cell Dynamics Research Center, Gwangju Institute of Science and Technology, Gwangju, South Korea.
S W NamDepartment of Pathology, College of Medicine, The Catholic University of Korea, Seoul, South Korea.
W KimDepartment of Molecular Science and Technology, Ajou University, Suwon, South Korea.
E K LeeDepartment of Biochemistry, College of Medicine, The Catholic University of Korea, Seoul, South Korea.
Catholic University of Korea · KRAjou University · KRHanyang University · KRGwangju Institute of Science and Technology · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

p130Cas regulates cancer progression by driving tyrosine receptor kinase signaling. Tight regulation of p130Cas expression is necessary for survival, apoptosis, and maintenance of cell motility in various cell types. Several studies revealed that transcriptional and post-translational control of p130Cas are important for maintenance of its expression and activity. To explore novel regulatory mechanisms of p130Cas expression, we studied the effect of microRNAs (miRs) on p130Cas expression in human breast cancer MCF7 cells. Here, we provide experimental evidence that miR-362-3p and miR-329 perform a tumor-suppressive function and their expression is downregulated in human breast cancer. miR-362-3p and miR-329 inhibited cellular proliferation, migration, and invasion, thereby suppressing tumor growth, by downregulating p130Cas. Ectopic expression of p130Cas attenuated the inhibitory effects of the two miRs on tumor progression. Relative expression levels of miR-362-3p/329 and p130Cas between normal and breast cancer correlated inversely; miR-362-3p/329 expression was decreased, whereas that of p130Cas increased in breast cancers. Furthermore, we showed that downregulation of miR-362-3p and miR-329 was caused by differential DNA methylation of miR genes. Enhanced DNA methylation (according to methylation-specific PCR) was responsible for downregulation of miR-362-3p and miR-329 in breast cancer. Taken together, these findings point to a novel role for miR-362-3p and miR-329 as tumor suppressors; the miR-362-3p/miR-329-p130Cas axis seemingly has a crucial role in breast cancer progression. Thus, modulation of miR-362-3p/miR-329 may be a novel therapeutic strategy against breast cancer.

Indexed as

Gene Expression Regulation, NeoplasticAnimalsBase SequenceBinding SitesBreast NeoplasmsCrk-Associated Substrate ProteinDisease ProgressionDown-RegulationFemaleGene ExpressionHumansMaleMCF-7 CellsMice, Inbred BALB CMice, NudeMicroRNAsCrk-Associated Substrate ProteinMicroRNAsMIRN329 microRNA, humanMIRN362 microRNA, human

Identifiers

PMID26337669
PMCPMC5072442
OpenAlexW2103380468

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.