Evidence map›Paper›PMID 24793789›Full record

ArticleOncogene2015

The MZF1/c-MYC axis mediates lung adenocarcinoma progression caused by wild-type lkb1 loss.

L-H Tsai, J-Y Wu, Y-W Cheng, C-Y Chen, G-T Sheu, T-C Wu, H Lee

Abstract 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. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
3.7field-weighted citation impact, top 6% 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

47 citing papers in PubMed, 80 citations in OpenAlex.

  1. Cancer discovery · 2018
    Trial
  2. Review
  3. Review
  4. Article
  5. The therapeutic potential of RNA m(6)A in lung cancer.Cell communication and signaling : CCS · 2024
    Review
  6. Ubiquitination and deubiquitination in the regulation of NJournal of molecular medicine (Berlin, Germany) · 2024
    Review
  7. Article
  8. Article
  9. Targeting MYC Regulation with Polypurine Reverse Hoogsteen Oligonucleotides.International journal of molecular sciences · 2022
    Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Review
  19. Article
  20. Review
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

7 authors at 5 institutions in 1 country.

L-H TsaiInstitute of Medicine, Chung Shan Medical University, Taichung, Taiwan.
J-Y WuDepartment of Surgery, Buddhist Tzu Chi General Hospital, Taichung Branch, and College of Medicine, Tzu Chi University, Hualien, Taiwan.
Y-W ChengGraduate Institute of Cancer Biology and Drug Discovery, College of Medical Science and Technology, Taipei Medical University, Taipei, Taiwan.
C-Y ChenDepartment of Surgery, China Medical University Hospital, Taichung, Taiwan.
G-T SheuInstitute of Medicine, Chung Shan Medical University, Taichung, Taiwan.
T-C WuDepartment of Internal Medicine, Chung Shan Medical University Hospital, Taichung, Taiwan.
H LeeGraduate Institute of Cancer Biology and Drug Discovery, College of Medical Science and Technology, Taipei Medical University, Taipei, Taiwan.
Chung Shan Medical University · TWTaipei Medical University · TWChina Medical University · TWChung Shan Medical University Hospital · TWTzu Chi University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Liver kinase B1 (LKB1) loss in lung adenocarcinoma is commonly caused by genetic mutations, but these mutations rarely occur in Asian patients. We recently reported wild-type LKB1 loss via the alteration of NKX2-1/p53-axis-promoted tumor aggressiveness and predicted poor outcomes in cases of lung adenocarcinoma. The mechanistic action of wild-type LKB1 loss within tumor progression remains unknown. The suppression of MYC by LKB1 controls epithelial organization; therefore, we hypothesize that MYC expression can be increased via wild-type LKB1 loss and promotes tumor progression. Here, MYC transcription is upregulated by LKB1-loss-mediated MZF1 expression. The wild-type LKB1-loss-mediated MZF1/MYC axis is responsible for soft-agar growth, migration and invasion in lung adenocarcinoma cells. Moreover, wild-type LKB1 loss-induced cell invasiveness was markedly suppressed by MYC inhibitors (10058-F4 and JQ1). Patients with low-LKB1/high-MZF1 or low-LKB1/high-MYC tumors have shorter overall survival and relapse-free-survival periods than patients with high-LKB1/low-MZF1 or high-LKB1/low-MYC tumors. In summary, MZF1-mediated MYC expression may promote tumor progression, resulting in poor outcomes in cases of lung adenocarcinoma with low-wild-type-LKB1 tumors.

Indexed as

AdenocarcinomaAdenocarcinoma of LungAMP-Activated Protein Kinase KinasesCell MovementDisease ProgressionHumansKruppel-Like Transcription FactorsLung NeoplasmsNeoplasm InvasivenessPromoter Regions, GeneticProtein Serine-Threonine KinasesProto-Oncogene Proteins c-mycAMP-Activated Protein Kinase KinasesKruppel-Like Transcription FactorsMYC protein, humanMZF1 protein, humanProtein Serine-Threonine KinasesProto-Oncogene Proteins c-mycSTK11 protein, human

Identifiers

PMID24793789
OpenAlexW2094809025

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.