Evidence map›Paper›PMID 31074594›Full record

ArticleCancer medicine2019

MicroRNA-4286 promotes cell proliferation, migration, and invasion via PTEN regulation of the PI3K/Akt pathway in non-small cell lung cancer.

Chunhua Ling, Xueting Wang, Jianjie Zhu, Haicheng Tang, Wenwen Du, Yuanyuan Zeng, Lin Sun, Jian-An Huang, Zeyi Liu

Open access · goldAbstract read
In one paragraph

Article in Cancer medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
3.4field-weighted citation impact, top 7% 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

33 citing papers in PubMed, 56 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Apelin/APJ: Another Player in the Cancer Biology Network.International journal of molecular sciences · 2025
    Review
  8. Review
  9. Review
  10. Review
  11. Article
  12. Review
  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

9 authors at 1 institution in 1 country.

Chunhua LingDepartment of Respiratory Medicine, the First Affiliated Hospital of Soochow University, Suzhou, China.
Xueting WangDepartment of Respiratory Medicine, the First Affiliated Hospital of Soochow University, Suzhou, China.
Jianjie ZhuDepartment of Respiratory Medicine, the First Affiliated Hospital of Soochow University, Suzhou, China.
Haicheng TangDepartment of Respiratory Medicine, the First Affiliated Hospital of Soochow University, Suzhou, China.
Wenwen DuDepartment of Respiratory Medicine, the First Affiliated Hospital of Soochow University, Suzhou, China.
Yuanyuan ZengDepartment of Respiratory Medicine, the First Affiliated Hospital of Soochow University, Suzhou, China.
Lin SunDepartment of Respiratory Medicine, the First Affiliated Hospital of Soochow University, Suzhou, China.
Jian-An HuangDepartment of Respiratory Medicine, the First Affiliated Hospital of Soochow University, Suzhou, China.
Zeyi LiuDepartment of Respiratory Medicine, the First Affiliated Hospital of Soochow University, Suzhou, China.ORCID 0000-0003-2528-6909
Soochow University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

It is well-known that phosphatase and tensin homologue deleted on chromosome 10 (PTEN) is a tumor suppressor which negatively regulates PI3K/AKT signaling and is activated widely in non-small cell lung cancers (NSCLC). However, genetic alterations in PTEN genes are rare, suggesting an undefined mechanism(s) for their suppression. Notably, growing evidence indicates that PTEN can be regulated by microRNAs involved in cancer progression. In this study, we discover that the miR-4286 is overexpressed in NSCLC and negatively regulates the expression of PTEN. Furthermore, we found that miR-4286 reduces PTEN expression by directly binding to PTEN 3'-untranslated region (UTR), thereby inhibiting NSCLC cell proliferation and mobility. Moreover, mechanistic investigations revealed that miR-4286 overexpression was a result of PTEN-mediated activation of the PI3K/AKT pathway. Taken together, our findings elucidate that miR-4286 promotes the tumorigenesis of NSCLC by interacting with PTEN. This miR-4286-mediated upregulation of PTEN might lead to new therapeutic strategies for NSCLC.

Indexed as

AgedAged, 80 and overApoptosisCarcinoma, Non-Small-Cell LungCell CycleCell Line, TumorCell MovementCell ProliferationEctopic Gene ExpressionFemaleGene Expression Regulation, NeoplasticHumansLung NeoplasmsMaleMicroRNAsMiddle AgedMicroRNAsMIRN-4286 microRNA, humanPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktPTEN PhosphohydrolasePTEN protein, humanmicroRNAmiR-4286non-small cell lung cancerphosphatase and tensin homologue deleted on chromosome 10PI3K/AKT signaling

Identifiers

PMID31074594
PMCPMC6601592
OpenAlexW2944460377

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.