Evidence map›Paper›PMID 25369201›Full record

ArticlePloS one2014

CDO, an Hh-coreceptor, mediates lung cancer cell proliferation and tumorigenicity through Hedgehog signaling.

Young-Eun Leem, Hye-Lim Ha, Ju-Hyeon Bae, Kwan-Hyuck Baek, Jong-Sun Kang

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.6field-weighted citation impact, top 33% 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

9 citing papers in PubMed, 15 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Cdon deficiency causes cardiac remodeling through hyperactivation of WNT/β-catenin signaling.Proceedings of the National Academy of Sciences of the United States of America · 2017
    Article
  7. A novel therapeutic approach against B-cell non-Hodgkin's lymphoma through co-inhibition of Hedgehog signaling pathway and autophagy.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Article
  8. Article
  9. 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

5 authors at 1 institution in 1 country.

Young-Eun LeemDepartment of Molecular Cell Biology, Sungkyunkwan University School of Medicine, Samsung Biomedical Research Institute, Suwon, 440-746, Republic of Korea.
Hye-Lim HaDepartment of Molecular Cell Biology, Sungkyunkwan University School of Medicine, Samsung Biomedical Research Institute, Suwon, 440-746, Republic of Korea.
Ju-Hyeon BaeDepartment of Molecular Cell Biology, Sungkyunkwan University School of Medicine, Samsung Biomedical Research Institute, Suwon, 440-746, Republic of Korea.
Kwan-Hyuck BaekDepartment of Molecular Cell Biology, Sungkyunkwan University School of Medicine, Samsung Biomedical Research Institute, Suwon, 440-746, Republic of Korea.
Jong-Sun KangDepartment of Molecular Cell Biology, Sungkyunkwan University School of Medicine, Samsung Biomedical Research Institute, Suwon, 440-746, Republic of Korea.
Samsung (South Korea) · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hedgehog (Hh) signaling plays essential roles in various developmental processes, and its aberrant regulation results in genetic disorders or malignancies in various tissues. Hyperactivation of Hh signaling is associated with lung cancer development, and there have been extensive efforts to investigate how to control Hh signaling pathway and regulate cancer cell proliferation. In this study we investigated a role of CDO, an Hh co-receptor, in non-small cell lung cancer (NSCLC). Inhibition of Hh signaling by SANT-1 or siCDO in lung cancer cells reduced proliferation and tumorigenicity, along with the decrease in the expression of the Hh components. Histological analysis with NSCLC mouse tissue demonstrated that CDO was expressed in advanced grade of the cancer, and precisely co-localized with GLI1. These data suggest that CDO is required for proliferation and survival of lung cancer cells via Hh signaling.

Indexed as

Cell ProliferationAnimalsApoptosisCarcinogenesisCell Adhesion MoleculesCell Line, TumorCell SurvivalFemaleHedgehog ProteinsHumansLung NeoplasmsMice, NudeNeoplasm StagingNeoplasm TransplantationSignal TransductionTranscription FactorsCDON protein, humanCell Adhesion MoleculesGLI1 protein, humanHedgehog ProteinsTranscription FactorsTumor Suppressor ProteinsZinc Finger Protein GLI1

Identifiers

PMID25369201
PMCPMC4219762
OpenAlexW2062439272

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.