Evidence map›Paper›PMID 24930499›Full record

ArticleOncotarget2014

Up-regulation of neogenin-1 increases cell proliferation and motility in gastric cancer.

Seok-Jun Kim, Yuan-Guo Wang, Hyun-Woo Lee, Hyeok Gu Kang, Sun-Hyuk La, Il Ju Choi, Tatsuro Irimura, Jae Y Ro, Robert S Bresalier, Kyung-Hee Chun

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

33 citing papers in PubMed, 58 citations in OpenAlex.

  1. Article
  2. Predictive capacity for local disease control of neogenin-1 (NEO1) transcriptional expression in patients with head and neck squamous cell carcinoma.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2025
    Article
  3. Article
  4. Review
  5. Research progress of the netrins and their receptors in cancer.Journal of cellular and molecular medicine · 2024
    Review
  6. Article
  7. Article
  8. Crosstalk between WNT and STAT3 is mediated by galectin-3 in tumor progression.Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 2021
    Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Oncology letters · 2018
    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

10 authors at 6 institutions in 3 countries.

Seok-Jun KimDepartment of Biochemistry and Molecular Biology, Yonsei University College of Medicine, Seoul, Republic of Korea.
Yuan-Guo Wang
Hyun-Woo Lee
Hyeok Gu Kang
Sun-Hyuk La
Il Ju Choi
Tatsuro Irimura
Jae Y Ro
Robert S Bresalier
Kyung-Hee Chun
Yonsei University · KRHarvard University Press · USMethodist Hospital · USNational Cancer Center · KRSt. Luke's International Hospital · JPThe University of Texas MD Anderson Cancer Center · US

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Scott Kopetz · 1985 to 2026
$290.8M
NCI NIH HHS P30 CA016672
6 · The paper itself

Abstract

Although elevated expression of neogenin-1 has been detected in human gastric cancer tissue, its role in gastric tumorigenesis remains unclear due to the lack of neogenin-1 studies in cancer. Therefore, we demonstrated here the function and regulatory mechanism of neogenin-1 in gastric cancer. Neogenin-1 ablation decreased proliferation and migration of gastric cancer cells, whereas its over-expression reversed these effects. Xenografted analyses using gastric cancer cells displayed statistically significant inhibition of tumor growth by neogenin-1 depletion. Interestingly, galectin-3 interacted with HSF-1 directly, which facilitated nuclear-localization and binding on neogenin-1 promoter to drive its transcription and gastric cancer cell motility. The galectin-3-increased gastric cancer cell motility was down-regulated by HSF-1 depletion. Moreover, the parallel expression patterns of galectin-3 and neogenin-1, as well as those of HSF-1 and neogenin-1, were detected in the malignant tissues of gastric cancer patients. Taken together, high-expression of neogenin-1 promotes gastric cancer proliferation and motility and its expression is regulated by HSF-1 and galectin-3 interaction. In addition, we propose further studies for neogenin-1 and its associated pathways to provide them as a proper target for gastric cancer therapy.

Indexed as

Cell MovementCell ProliferationAdenocarcinomaAnimalsBlotting, WesternCell Line, TumorDNA-Binding ProteinsGalectin 3Gene Expression Regulation, NeoplasticHeat Shock Transcription FactorsHeterograftsHumansImmunoprecipitationMembrane ProteinsMiceReverse Transcriptase Polymerase Chain ReactionDNA-Binding ProteinsGalectin 3Heat Shock Transcription FactorsMembrane ProteinsneogeninRNA, Small InterferingTranscription Factors

Identifiers

PMID24930499
PMCPMC4102817
OpenAlexW1571071480

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.