Evidence map›Paper›PMID 27250766›Full record

ArticleScientific reports2016

Hypoxia induced CCL28 promotes angiogenesis in lung adenocarcinoma by targeting CCR3 on endothelial cells.

Guichun Huang, Leilei Tao, Sunan Shen, Longbang Chen

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
1.6field-weighted citation impact, top 15% 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

40 citing papers in PubMed, 63 citations in OpenAlex.

  1. Observational
  2. Mutant KRAS in brain endothelial cells promotes vascular inflammation and impairs vascular integrity in brain arteriovenous malformation.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2026
    Article
  3. Article
  4. The Significance of CXCL1 in Cancer: An Overview of Molecular Mechanisms.International journal of molecular sciences · 2026
    Review
  5. Review
  6. An Increase in the Chemokine Mediators (CCL28 and CCR10) Associated with the Progression of Oral Squamous Cell Carcinoma: A Cross-Sectional Investigation.Indian journal of otolaryngology and head and neck surgery : official publication of the Association of Otolaryngologists of India · 2024
    Article
  7. Article
  8. Review
  9. Article
  10. CCR3-dependent eosinophil recruitment is regulated by sialyltransferase ST3Gal-IV.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  11. Review
  12. Article
  13. Article
  14. Targeting Angiogenesis via Resolution of Inflammation.Cold Spring Harbor perspectives in medicine · 2023
    Review
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. 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

4 authors at 2 institutions in 1 country.

Guichun HuangMedical Oncology Department of Jinling Hospital, Medical School of Nanjing University, Nanjing, China.
Leilei TaoMedical Oncology Department of Jinling Hospital, Medical School of Nanjing University, Nanjing, China.
Sunan ShenMedical School of Nanjing University, Nanjing, China.
Longbang ChenMedical Oncology Department of Jinling Hospital, Medical School of Nanjing University, Nanjing, China.
Nanjing General Hospital of Nanjing Military Command · CNNanjing University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tumor hypoxia is one of the important features of lung adenocarcinoma. Chemokines might mediate the effects caused by tumor hypoxia. As confirmed in tumor tissue and serum of patients, CC chemokine 28 (CCL28) was the only hypoxia induced chemokine in lung adenocarcinoma cells. CCL28 could promote tube formation, migration and proliferation of endothelial cells. In addition, angiogenesis was promoted by CCL28 in the chick chorioallantoic membrane and matrigel implanted in dorsal back of athymic nude mice (CByJ.Cg-Foxn1(nu)/J). Tumors formed by lung adenocarcinoma cells with high expression of CCL28 grew faster and had a higher vascular density, whereas tumor formation rate of lung adenocarcinoma cells with CCL28 expression knockdown was quite low and had a lower vascular density. CCR3, receptor of CCL28, was highly expressed in vascular endothelial cells in lung adenocarcinoma when examining by immunohistochemistry. Further signaling pathways in endothelial cells, modulated by CCL28, were analyzed by Phosphorylation Antibody Array. CCL28/CCR3 signaling pathway could bypass that of VEGF/VEGFR on the levels of PI3K-Akt, p38 MAPK and PLC gamma. The effects could be neutralized by antibody against CCR3. In conclusion, CCL28, as a chemokine induced by tumor hypoxia, could promote angiogenesis in lung adenocarcinoma through targeting CCR3 on microvascular endothelial cells.

Indexed as

Up-RegulationA549 CellsAdenocarcinomaAdenocarcinoma of LungAdultAgedAnimalsCell HypoxiaCell MovementCell ProliferationChemokines, CCFemaleHumansHuman Umbilical Vein Endothelial CellsLung NeoplasmsMaleCCL28 protein, humanCCR3 protein, humanChemokines, CCReceptors, CCR3

Identifiers

PMID27250766
PMCPMC4890017
OpenAlexW2417009562

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.