Evidence map›Paper›PMID 24998847›Full record

ArticleOncogene2015

FHIT loss confers cisplatin resistance in lung cancer via the AKT/NF-κB/Slug-mediated PUMA reduction.

D-W Wu, M-C Lee, N-Y Hsu, T-C Wu, J-Y Wu, Y-C Wang, Y-W Cheng, C-Y Chen, H Lee

Erratum issuedOpen access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

29 citing papers in PubMed, 61 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Review
  6. Review
  7. Article
  8. International journal of molecular sciences · 2023
    Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 5 institutions in 1 country.

D-W WuGraduate Institute of Cancer Biology and Drug Discovery, College of Medical Science and Technology, Taipei Medical University, Taipei, Taiwan, ROC.
M-C LeeDivision of Thoracic Surgery, Department of Surgery, Taichung Veterans General Hospital, Taichung, Taiwan, ROC.
N-Y HsuGraduate Institute of Cancer Biology and Drug Discovery, College of Medical Science and Technology, Taipei Medical University, Taipei, Taiwan, ROC.
T-C Wu1] Division of Chest Medicine, Chung Shan Medical University Hospital, Taichung, Taiwan, ROC [2] School of Medicine, Chung Shan Medical University, Taichung, Taiwan, ROC.
J-Y Wu1] Division of Thoracic Surgery, Buddhist Tzu Chi General Hospital, Taichung Branch, Taichung, Taiwan, ROC [2] Department of Medicine, Tzu Chi University, Hualien, Taiwan, ROC.
Y-C Wang1] Division of Chest Medicine, Chung Shan Medical University Hospital, Taichung, Taiwan, ROC [2] School of Medicine, Chung Shan Medical University, Taichung, Taiwan, ROC.
Y-W ChengGraduate Institute of Cancer Biology and Drug Discovery, College of Medical Science and Technology, Taipei Medical University, Taipei, Taiwan, ROC.
C-Y ChenDepartment of Surgery, China Medical University Hospital, Taichung, Taiwan, ROC.
H LeeGraduate Institute of Cancer Biology and Drug Discovery, College of Medical Science and Technology, Taipei Medical University, Taipei, Taiwan, ROC.
Taipei Medical University · TWChung Shan Medical University Hospital · TWBuddhist Tzu Chi General Hospital · TWChina Medical University Hospital · TWTaichung Veterans General Hospital · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Fragile histidine triad (FHIT) loss by the two-hit mechanism of loss of heterozygosity and promoter hypermethylation commonly occurrs in non-small cell lung cancer (NSCLC) and may confer cisplatin resistance in NSCLC cells. However, the underlying mechanisms of FHIT loss in cisplatin resistance and the response to cisplatin-based chemotherapy in NSCLC patients have not yet been reported. In the present study, inhibition concentration of 50% cell viability induced by cisplatin (IC50) and soft agar growth and invasion capability were increased and decreased in FHIT-knockdown and -overexpressing cells, respectively. Mechanistically, Slug transcription is upregulated by AKT/NF-κB activation due to FHIT loss and, in turn, Slug suppresses PUMA expression; this decrease of PUMA by FHIT loss is responsible for cisplatin resistance. In addition, cisplatin resistance due to FHIT loss can be conquered by AKT inhibitor-perifosine in xenograft tumors. Among NSCLC patients, low FHIT, high p-AKT, high Slug and low PUMA were correlated with shorter overall survival, relapse-free survival and poorer response to cisplatin-based chemotherapy. Therefore, the AKT inhibitor perifosine might potentially overcome the resistance to cisplatin-based chemotherapy in NSCLC patients with low-FHIT tumors, and consequently improve the outcome.

Indexed as

Acid Anhydride HydrolasesAdultAgedAged, 80 and overAnimalsAntineoplastic AgentsApoptosisApoptosis Regulatory ProteinsBis(5'-adenosyl)triphosphataseCarcinoma, Non-Small-Cell LungCisplatinDrug Resistance, NeoplasmFemaleHumansLung NeoplasmsMale3-(4-methylphenylsulfonyl)-2-propenenitrileAcid Anhydride HydrolasesAntineoplastic AgentsApoptosis Regulatory ProteinsBBC3 protein, humanBis(5'-adenosyl)triphosphataseCisplatinNeoplasm ProteinsNitrilesperifosinePhosphorylcholineProto-Oncogene ProteinsProto-Oncogene Proteins c-aktRNA, Small InterferingSNAI1 protein, humanSnai2 protein, mouseSnail Family Transcription FactorsSulfonesTranscription Factor RelATranscription Factors

Identifiers

PMID24998847
OpenAlexW2014565367

What OpenQuestion holds

Textmetadata
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.