Evidence map›Paper›PMID 25814287›Full record

ArticleMedical oncology (Northwood, London, England)2015

Norcantharidin inhibits Wnt signal pathway via promoter demethylation of WIF-1 in human non-small cell lung cancer.

Junran Xie, Yaping Zhang, Xuming Hu, Ran Lv, Dongju Xiao, Li Jiang, Qi Bao

Abstract read
PubMed Publisher
In one paragraph

Article in Medical oncology (Northwood, London, England), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 1 pooled it
1.6field-weighted citation impact, top 18% 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

16 citing papers in PubMed, 1 synthesis or guideline pooled it, 33 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Review
  5. Article
  6. Review
  7. Article
  8. Hypermethylation ofOncology letters · 2018
    Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Norcantharidin induces autophagy-related prostate cancer cell death through Beclin-1 upregulation by miR-129-5p suppression.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Article
  15. Article
  16. Norcantharidin modulates miR-655-regulated SENP6 protein translation to suppresses invasion of glioblastoma cells.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    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

7 authors at 4 institutions in 1 country.

Junran XieDepartment of Anesthesiology, Sir Run Run Shaw Hospital, Zhejiang University School of Medicine, 3 Eastern Qingchun Road, Hangzhou, 310016, People's Republic of China, junranxie@163.com.
Yaping Zhang
Xuming Hu
Ran Lv
Dongju Xiao
Li Jiang
Qi Bao
Sir Run Run Shaw Hospital · CNXuzhou Medical College · CNZhejiang University · CNXuzhou University of Technology · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Wingless-type (Wnt) family of secreted glycoproteins is a group of signal molecules implicated in oncogenesis. Abnormal activation of Wnt signal pathway is associated with a variety of human cancers, including non-small cell lung cancer (NSCLC). Wnt antagonists, such as the secreted frizzled-related protein (SFRP) family, Wnt inhibitory factor-1 (WIF-1) and cerberus, inhibit Wnt signal pathway by directly binding to Wnt molecules. Norcantharidin (NCTD) is known to possess anticancer activity but less nephrotoxicity than cantharidin. In this study, we found that NCTD inhibited cell proliferation, induced apoptosis, arrested cell cycle and suppressed cell invasion/migration in vitro. Additionally, Wnt signal pathway transcription was also suppressed. NCTD treatment blocked cytoplasmic translocation of beta-catenin into the nucleus. Alterations of apoptosis-related proteins, such as Bax, cleaved caspase-3 (pro-apoptotic) and Bcl-2 (anti-apoptotic), had been detected. Furthermore, the expression levels of WIF-1 and SFRP1 were significantly increased in NCTD-treated groups compared with negative control (NC) groups. Abnormal methylation was observed in NC groups, while NCTD treatment promoted WIF-1 demethylation. The present study revealed that NCTD activated WIF-1 via promoter demethylation, inhibiting the canonical Wnt signal pathway in NSCLC, which may present a new therapeutic target in vivo.

Indexed as

Adaptor Proteins, Signal TransducingApoptosisbcl-2-Associated X Proteinbeta CateninBridged Bicyclo Compounds, HeterocyclicCarcinoma, Non-Small-Cell LungCaspase 3Cell Cycle CheckpointsCell Line, TumorCell MovementCell ProliferationDNA MethylationHumansIntercellular Signaling Peptides and ProteinsLung NeoplasmsMembrane ProteinsAdaptor Proteins, Signal Transducingbcl-2-Associated X Proteinbeta CateninBridged Bicyclo Compounds, HeterocyclicCaspase 3Intercellular Signaling Peptides and ProteinsMembrane ProteinsnorcantharidinProto-Oncogene Proteins c-bcl-2Repressor ProteinsSecreted Frizzled-Related ProteinsSFRP1 protein, humanWIF1 protein, human

Identifiers

PMID25814287
OpenAlexW2034899078

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.