Evidence map›Paper›PMID 25342548›Full record

ArticleMolecular cancer2014

Pim-1 kinase is a target of miR-486-5p and eukaryotic translation initiation factor 4E, and plays a critical role in lung cancer.

Wenshuai Pang, Xin Tian, Fan Bai, Ruiyu Han, Juan Wang, Haitao Shen, Xianghong Zhang, Yueping Liu, Xia Yan, Feng Jiang and 1 more

Open access · goldAbstract read
In one paragraph

Article in Molecular cancer, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
5.1field-weighted citation impact, top 4% 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

41 citing papers in PubMed, 62 citations in OpenAlex.

  1. A Robust NSCLC Biomarker- miR-7-5p: ItsMicroRNA (Shariqah, United Arab Emirates) · 2025
    Article
  2. Article
  3. PIM1 kinase and its diverse substrate in solid tumors.Cell communication and signaling : CCS · 2024
    Review
  4. Targeting BET Proteins Downregulates miR-33a To Promote Synergy with PIM Inhibitors in CMML.Clinical cancer research : an official journal of the American Association for Cancer Research · 2023
    Article
  5. Review
  6. MicroRNA in adenoid cystic carcinoma (Review).International journal of oncology · 2023
    Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. MicroRNA-486-5p Suppresses Lung CancerFrontiers in oncology · 2021
    Article
  12. Frontiers of MicroRNA Signature in Non-small Cell Lung Cancer.Frontiers in cell and developmental biology · 2021
    Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Review
  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

11 authors at 3 institutions in 2 countries.

Wenshuai Pang
Xin Tian
Fan Bai
Ruiyu Han
Juan Wang
Haitao Shen
Xianghong Zhang
Yueping Liu
Xia Yan
Feng Jiang
Lingxiao XingDepartment of Pathology, Hebei Medical University, Shijiazhuang, Hebei, China. xinglingxiao@hotmail.com.
Hebei Medical University · CNFourth Hospital of Hebei Medical University · CNUniversity of Maryland, Baltimore · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundPim-1 kinase is a proto-oncogene and its dysregulation contributes to tumorigenesis and progression of a variety of malignancies. Pim-1 was suggested as a therapeutic target of cancers. The functional relevance of Pim-1 and the mechanism underlying its dysregulation in lung tumorigenesis remained unclear. This study aimed to investigate if Pim-1 has important functions in non-small-cell lung cancer (NSCLC) by: 1) evaluating the clinicopathologic significance of Pim-1 through analysing its expression in 101 human NSCLCs tissues using quantitative PCR, Western Blot and immunohistochemical studies, 2) determining its role in NSCLC and drug resistance using in vitro assays, and 3) investigating the regulatory mechanism of Pim-1 dysregulation in lung tumorigenesis.

resultsPim-1 was upregulated in 66.2% of the lung tumor tissues and its expression was significantly related to advanced stage (P = 0.019) and lymph node metastasis (P = 0.026). Reduced Pim-1 expression suppressed NSCLC cell growth, cell cycle progression and migration in vitro. Pim-1 was a novel target of miR-486-5p determined by luciferase report assay, and ectopic miR-486-5p expression in cancer cells reduced Pim-1 expression. Furthermore, eukaryotic translation initiation factor 4E (eIF4E) controlled the synthesis of Pim-1 in NSCLC cells, and its expression was positively associated with that of Pim-1 in NSCLC tissue specimens (r = 0.504, p < 0.001). The downregulated miR-486-5p and upregulated eIF4E in NSCLC cells led to the overexpression of Pim-1 by relieving the inhibitory effect of the 3'-UTR or 5'-UTR of Pim-1 mRNA, respectively. Moreover, Pim-1 knockdown sensitized NSCLC cells to cisplatin and EGFR tyrosine kinase inhibitor, gefitinib.

conclusionsPim-1 kinase could be a critical survival signaling factor in NSCLC, and regulated by miR-486-5p and eIF4E. Pim-1 kinase may provide a potential target for diagnosis and treatment for lung cancer.

Indexed as

AgedCarcinoma, Non-Small-Cell LungCell CycleCell Line, TumorCell MovementCell ProliferationCisplatinEukaryotic Initiation Factor-4EFemaleGefitinibGene Expression Regulation, NeoplasticGene Knockdown TechniquesHumansLung NeoplasmsMaleMicroRNAsCisplatinEukaryotic Initiation Factor-4EGefitinibMAS1 protein, humanMicroRNAsMIRN486 microRNA, humanProto-Oncogene MasProto-Oncogene Proteins c-pim-1Quinazolines

Identifiers

PMID25342548
PMCPMC4213487
OpenAlexW2149523454

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.