Evidence map›Paper›PMID 28878284›Full record

ArticleScientific reports2017

MicroRNA-449a deficiency promotes colon carcinogenesis.

Masanori Niki, Kohei Nakajima, Daichi Ishikawa, Jun Nishida, Chieko Ishifune, Shin-Ichi Tsukumo, Mitsuo Shimada, Shinji Nagahiro, Yoshinori Mitamura, Koji Yasutomo

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.5field-weighted citation impact, top 37% 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

10 citing papers in PubMed, 15 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. Article
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 1 institution in 1 country.

Masanori NikiDepartment of Immunology & Parasitology, Graduate School of Medicine, Tokushima University, Tokushima, Japan.
Kohei NakajimaDepartment of Immunology & Parasitology, Graduate School of Medicine, Tokushima University, Tokushima, Japan.
Daichi IshikawaDepartment of Immunology & Parasitology, Graduate School of Medicine, Tokushima University, Tokushima, Japan.
Jun NishidaDepartment of Immunology & Parasitology, Graduate School of Medicine, Tokushima University, Tokushima, Japan.
Chieko IshifuneDepartment of Immunology & Parasitology, Graduate School of Medicine, Tokushima University, Tokushima, Japan.
Shin-Ichi TsukumoDepartment of Immunology & Parasitology, Graduate School of Medicine, Tokushima University, Tokushima, Japan.
Mitsuo ShimadaDepartment of Surgery, Graduate School of Medicine, Tokushima University, Tokushima, Japan.
Shinji NagahiroDepartment of Neurosurgery, Graduate School of Medicine, Tokushima University, Tokushima, Japan.
Yoshinori MitamuraDepartment of Ophthalmology, Graduate School of Medicine, Tokushima University, Tokushima, Japan.
Koji YasutomoDepartment of Immunology & Parasitology, Graduate School of Medicine, Tokushima University, Tokushima, Japan. yasutomo@tokushima-u.ac.jp.
Tokushima University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

MicroRNAs have broad roles in tumorigenesis and cell differentiation through regulation of target genes. Notch signaling also controls cell differentiation and tumorigenesis. However, the mechanisms through which Notch mediates microRNA expression are still unclear. In this study, we aimed to identify microRNAs regulated by Notch signaling. Our analysis found that microRNA-449a (miR-449a) was indirectly regulated by Notch signaling. Although miR-449a-deficient mice did not show any Notch-dependent defects in immune cell development, treatment of miR-449a-deficient mice with azoxymethane (AOM) or dextran sodium sulfate (DSS) increased the numbers and sizes of colon tumors. These effects were associated with an increase in intestinal epithelial cell proliferation following AOM/DSS treatment. In patients with colon cancer, miR-449a expression was inversely correlated with disease-free survival and histological scores and was positively correlated with the expression of MLH1 for which loss-of function mutations have been shown to be involved in colon cancer. Colon tissues of miR-449a-deficient mice showed reduced Mlh1 expression compared with those of wild-type mice. Thus, these data suggested that miR-449a acted as a key regulator of colon tumorigenesis by controlling the proliferation of intestinal epithelial cells. Additionally, activation of miR-449a may represent an effective therapeutic strategy and prognostic marker in colon cancer.

Indexed as

Gene Expression Regulation, NeoplasticGenetic Predisposition to DiseaseAnimalsBiomarkersBiomarkers, TumorCell Line, TumorCell ProliferationCell Transformation, NeoplasticColonic NeoplasmsGene Expression ProfilingImmunophenotypingMiceMice, KnockoutMice, TransgenicMicroRNAsMutL Protein Homolog 1BiomarkersBiomarkers, TumorMicroRNAsMirn449 microRNA, mouseMLH1 protein, humanMutL Protein Homolog 1Receptors, Notch

Identifiers

PMID28878284
PMCPMC5587792
OpenAlexW2753603018

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.