Evidence map›Paper›PMID 30569167›Full record

ArticleMolecular medicine reports2019

MiR‑495 suppresses cell proliferation by directly targeting HMGA2 in lung cancer.

Jiangtao Sun, Yanping Qiao, Tao Song, Haiwen Wang

Abstract read
In one paragraph

Article in Molecular medicine reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
–field-weighted citation impact
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

17 citing papers in PubMed.

  1. Article
  2. Review
  3. MicroRNA-495: a therapeutic and diagnostic tumor marker.Journal of molecular histology · 2023
    Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. NFAT5, which protects against hypertonicity, is activated by that stress via structuring of its intrinsically disordered domain.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  15. Article
  16. Article
  17. OncoTargets and therapy · 2020
    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.

Jiangtao SunDepartment of Oncology, Weihai Central Hospital, Weihai, Shandong 264400, P.R. China.
Yanping QiaoDepartment of Hematology, Weihai Central Hospital, Weihai, Shandong 264400, P.R. China.
Tao SongDepartment of Endocrinology, Weihai Central Hospital, Weihai, Shandong 264400, P.R. China.
Haiwen WangDepartment of Cardio‑Thoracic Surgery, Weihai Central Hospital, Weihai, Shandong 264400, P.R. China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The present study aimed to investigate the expression of microRNA‑495 (miR‑495) in non‑small cell lung cancer (NSCLC) tissues and cells, as well as its function on the proliferation of lung cancer cells. The expression of miR‑495 in 122 pairs of NSCLC tissues and matched paracarcinoma tissues, as well as in human lung cancer cell lines (A549, H460, H1650, H520 and SK‑MES‑1) and the normal human pulmonary bronchial epithelial cell line 16HBE was determined using reverse transcription quantitative polymerase chain reaction (RT‑qPCR). As predicted by bioinformatics analysis, high mobility group A2 (HMGA2) may be a potential target gene of miR‑495. In addition, the regulatory function of miR‑495 on its target gene HMGA2 was evaluated using a dual‑luciferase reporter assay, RT‑qPCR and western blotting. Furthermore, the effect of miR‑495 on the proliferation of A549 lung cancer cells was investigated using a Cell Counting Kit‑8 (CCK‑8) assay. The results demonstrated that the expression of miR‑495 in NSCLC tissues and cells was significantly downregulated compared with the control. In addition, downregulated expression of miR‑495 was associated with tumor differentiation, lymph node metastasis and tumor, node and metastasis staging. Additionally, a dual‑luciferase reporter assay revealed that miR‑495 could directly associated with the 3'‑untranslated region of HMGA2. Upregulated expression of miR‑495 significantly downregulated the mRNA and protein expression levels of HMGA2 in A549 cells. Furthermore, the results of CCK‑8 assay revealed that upregulated expression of miR‑495 significantly suppressed the proliferation of A549 cells; HMGA2 overexpression reversed this inhibition. In summary, the findings of the present study demonstrated that miR‑495 was downregulated in NSCLC tissues and cells. In addition, miR‑495 suppressed the proliferation of lung cancer cells by directly targeting HMGA2.

Indexed as

A549 CellsBronchiCell ProliferationEpithelial CellsEpithelial-Mesenchymal TransitionGene Expression Regulation, NeoplasticHMGA2 ProteinHumansLung NeoplasmsLymphatic MetastasisMicroRNAsHMGA2 ProteinHMGA2 protein, humanMicroRNAsMIRN495 microRNA, humanhigh mobility group AT-hook 2lung cancermicroRNA-495proliferation

Identifiers

PMID30569167
PMCPMC6390076

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.