Evidence map›Paper›PMID 24228711›Full record

ArticleCancer cell international2013

Wilms' tumour suppressor gene 1 (WT1) is involved in the carcinogenesis of Lung cancer through interaction with PI3K/Akt pathway.

Xi Wang, Ping Gao, Fang Lin, Min Long, Yuanyuan Weng, Yongri Ouyang, Li Liu, Junxia Wei, Xi Chen, Ting He and 2 more

Open access · goldAbstract read
In one paragraph

Article in Cancer cell international, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.3field-weighted citation impact, top 19% 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

15 citing papers in PubMed, 28 citations in OpenAlex.

  1. Article
  2. Frontiers in pharmacology · 2026
    Article
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  4. Article
  5. Review
  6. Article
  7. Genetic Polymorphisms of theJournal of kidney cancer and VHL · 2021
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. 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

12 authors at 1 institution in 1 country.

Xi Wang
Ping Gao
Fang Lin
Min Long
Yuanyuan Weng
Yongri Ouyang
Li Liu
Junxia Wei
Xi Chen
Ting He
Huizhong ZhangDepartment of Clinical Diagnosis, Tangdu Hospital, Fourth Military Medical University, Xi'an, China. zhzcenter@aliyun.com.
Ke Dong
Air Force Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

absractAlthough studies have shown the oncogene WT1 is overexpressed in lung cancer, there is no data showing the implication of WT1 in lung cancer biology. In the present study, we first demonstrated that isotype C of WT1 was conservely overexpressed in 20 lung cancer patient specimens. Knockdown of WT1 by small interference RNA (siRNA) transfection resulted in a significant inhibition of cell proliferation, induction of cell cycle arrest at G1 phase, and the expression change of BCL-2 family genes in WT1+ A549 cells. Furthermore, we found that DDP treatment could decrease the WT1 mRNA expression level by 5% and 15% at a dose of 1 μg/ml, by 25% and 40% at a dose of 2 μg/ml for 24 and 48 h, respectively. In the mean time, DDP treatment also reduced the PI3K/AKT pathway activity. Further analysis by using siRNA targeting the AKT-1 and the PI3K pathway inhibitor Ly294002 revealed that the AKT-1 siRNA reduced the WT1 expression effectively in A549 cells, and the same result was observed in Ly294002 treated cells, indicating that DDP treatment could down regulate WT1 expression through the PI3K/AKT pathway. Of particular interest, knockdown of WT1 also inhibited the AKT expression effectively, Chip assay further confirmed that WT1 is a transcription factor of AKT-1. We thus concluded that there is a positive feedback loop between WT1 and AKT-1. Taken together, DDP treatment downregulates the WT1 expression through the PI3K/AKT signaling pathway, and there is a feedback between WT1 and AKT-1; WT1 is involved in cellular proliferation in A549 cells, WT1 inhibition in combination with DDP will provide a new light for lung cancer therapy.

Identifiers

PMID24228711
PMCPMC3833182
OpenAlexW2128658297

What OpenQuestion holds

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Registered trials

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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.