Evidence map›Paper›PMID 28000891›Full record

ArticleMolecular medicine reports2017

Expression of miR‑26a exhibits a negative correlation with HMGA1 and regulates cancer progression by targeting HMGA1 in lung adenocarcinoma cells.

Noboru Sekimoto, Ayako Suzuki, Yutaka Suzuki, Sumio Sugano

Open access · hybridAbstract read
In one paragraph

Article in Molecular medicine reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

18 citing papers in PubMed, 23 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Prognostic Significance ofInternational journal of molecular sciences · 2022
    Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. HMGA Genes and Proteins in Development and Evolution.International journal of molecular sciences · 2020
    Review
  13. Clinical Implications of Extracellular HMGA1 in Breast Cancer.International journal of molecular sciences · 2019
    Review
  14. Article
  15. Article
  16. Review
  17. [MicroRNA-26a and Tumor].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2017
    Review
  18. 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

4 authors at 2 institutions in 1 country.

Noboru SekimotoDepartment of Computational Biology and Medical Sciences, Graduate School of Frontier Sciences, The University of Tokyo, Tokyo 108‑8639, Japan.
Ayako SuzukiDivision of Translational Research, Exploratory Oncology Research and Clinical Trial Center, National Cancer Center, Kashiwa, Chiba 277‑8577, Japan.
Yutaka SuzukiDepartment of Computational Biology and Medical Sciences, Graduate School of Frontier Sciences, The University of Tokyo, Kashiwa, Chiba 277‑8562, Japan.
Sumio SuganoDepartment of Computational Biology and Medical Sciences, Graduate School of Frontier Sciences, The University of Tokyo, Tokyo 108‑8639, Japan.
The University of Tokyo · JPChiba Cancer Center · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lung cancer is the most common cause of cancer‑associated mortality worldwide, and the number of cases is increasing annually. Several studies have shown that microRNAs (miRNAs) control proliferation, differentiation, and apoptosis in various cell types, and increasing evidence indicates the presence of aberrant miRNA expression profiles and unique miRNA signaling pathways in several types of cancer. The present study aimed to identify miRNAs, which correlated specifically with the progression of lung cancer through the analysis of 57,100 transcripts and 1,341 small RNA expression profiles in 26 lung adenocarcinoma cell lines using next‑generation sequencing. The most marked negative correlation was found between the expression of hsa‑miR‑26a‑1 and messenger RNA (mRNA), and a list of mRNAs, which exhibited negative correlation with hsa‑miR‑26a‑1 were investigated. The most marked negative correlation was observed between the expression levels of hsa‑miR‑26a‑1 and high mobility group A1 (HMGA1). Using a lung adenocarcinoma cell line, the present study analyzed the effect of the overexpression of miR‑26a on the expression of HMGA1 and found that miR‑26a repressed the expression of HMGA1 by reducing the mRNA levels of HMGA1. Furthermore, it was demonstrated that the overexpression of miR‑26a in a lung adenocarcinoma cell line repressed cell migration, invasion and growth by targeting HMGA1. Taken together, the present study showed a significant negative correlation between the expression of miR‑26a and HMGA1 in 26 lung adenocarcinoma cell lines, and provided evidence that the suppression of miR‑26a supports the progression of cancer by stimulating the expression of HMGA1.

Indexed as

3' Untranslated RegionsBase SequenceCell Line, TumorCell MovementCell ProliferationHMGA1a ProteinHumansLung NeoplasmsMicroRNAsPTEN PhosphohydrolaseRNA InterferenceRNA, MessengerRNA, Small InterferingSequence AlignmentTranscriptome3' Untranslated RegionsHMGA1a ProteinMicroRNAsPTEN PhosphohydrolaseRNA, MessengerRNA, Small Interfering

Identifiers

PMID28000891
PMCPMC5364888
OpenAlexW2564802602

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.