Evidence map›Paper›PMID 30628663›Full record

ArticleInternational journal of molecular medicine2019

miR‑505 inhibits cell growth and EMT by targeting MAP3K3 through the AKT‑NFκB pathway in NSCLC cells.

Huaping Tang, Weihong Lv, Wenxin Sun, Qiaojie Bi, Yueqin Hao

Open access · hybridAbstract read
In one paragraph

Article in International journal of molecular medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
0.9field-weighted citation impact, top 31% 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

20 citing papers in PubMed, 21 citations in OpenAlex.

  1. EML4-ALK fusion rewires transcriptomic, miRNA, and CAF-associated programs in non-small cell lung cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
    Article
  2. Article
  3. NF-κB in inflammation and cancer.Cellular & molecular immunology · 2025
    Review
  4. Article
  5. Review
  6. Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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

5 authors at 2 institutions in 1 country.

Huaping TangDepartment of Respiration, Qingdao Municipal Hospital, Qingdao, Shandong 266071, P.R. China.
Weihong LvDepartment of Medical, Qingdao Municipal Hospital, Qingdao, Shandong 266071, P.R. China.
Wenxin SunDepartment of Respiration, Qingdao Municipal Hospital, Qingdao, Shandong 266071, P.R. China.
Qiaojie BiDepartment of Emergency, Qingdao Municipal Hospital, Qingdao, Shandong 266071, P.R. China.
Yueqin HaoDepartment of Respiration, Qingdao Municipal Hospital, Qingdao, Shandong 266071, P.R. China.
Qingdao Municipal Hospital · CNQingdao University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

MicroRNAs (miRNAs) are short non‑coding RNAs, which generally regulate gene expression at the post‑transcriptional level. Dysregulation of miRNAs has been reported in numerous cancer types, including lung cancer. In the present study, the role of miR‑505 in non‑small cell lung cancer (NSCLC) cells was investigated. miR‑505 served a tumor suppressor role in NSCLC cells. By reverse transcriptase‑quantitative polymerase chain reaction detection, it was demonstrated that miR‑505 was downregulated in NSCLC tissues and cell lines, which is negatively associated with large tumor size, Tumor‑Node‑Metastasis stage and distant metastasis in patients with NSCLC. Functional studies revealed that miR‑505 inhibited cell proliferation, migration, invasion and epithelial‑mesenchymal transition progress in vitro and tumor growth in vivo. Mechanically, mitogen‑activated protein kinase kinase kinase 3 (MAP3K3) was identified as a direct target of miR‑505 by binding to its 3'untranslated region and demonstrated to mediate the tumor suppressor roles of miR‑505 in NSCLC cells. The effect of miR‑505 on the activation of AKT/nuclear factor‑κB (NFκB) pathway, which was downstream targets of MAP3K3, was further analyzed by western blot analysis and immunofluorescence analyses. The data demonstrated the inhibition of the AKT/NFκB pathway upon overexpressing miR‑505 and the activation of AKT/NFκB pathway upon silencing miR‑505. Collectively, the data revealed the novel role and target of miR‑505 in NSCLC cells, which may provide novel insights regarding its role in the carcinogenesis of NSCLC and its potential values for clinical applications.

Indexed as

AdultAgedAnimalsCarcinoma, Non-Small-Cell LungCell CycleCell Line, TumorCell MovementCell ProliferationEpithelial-Mesenchymal TransitionFemaleGene Expression Regulation, NeoplasticGenes, ReporterHumansLung NeoplasmsMAP Kinase Kinase Kinase 3MiceMAP3K3 protein, humanMAP Kinase Kinase Kinase 3MicroRNAsMIRN505 microRNA, humanNF-kappa BProto-Oncogene Proteins c-akt

Identifiers

PMID30628663
PMCPMC6365022
OpenAlexW2907986716

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.