Evidence map›Paper›PMID 29257333›Full record

ArticleMolecular medicine reports2018

COX‑2 inhibition in the endothelium induces glucose metabolism normalization and impairs tumor progression.

Longhui Zhang, Sufen Li, Lan Li, Zhengqiong Chen, Ying Yang

Open access · hybridAbstract read
In one paragraph

Article in Molecular medicine reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
0.7field-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

19 citing papers in PubMed, 21 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Dietary fat and lipid metabolism in the tumor microenvironment.Biochimica et biophysica acta. Reviews on cancer · 2023
    Review
  6. Review
  7. Review
  8. Article
  9. Review
  10. Metabolic Reprogramming in Tumor Endothelial Cells.International journal of molecular sciences · 2022
    Review
  11. Review
  12. Article
  13. Review
  14. Review
  15. Tumor Endothelial Cell-A Biological Tool for Translational Cancer Research.International journal of molecular sciences · 2020
    Review
  16. Article
  17. Review
  18. Article
  19. Review
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 3 institutions in 1 country.

Longhui ZhangObstetrics and Gynecology Department, Xinqiao Hospital, Third Military Medical University, Chongqing 400037, P.R. China.
Sufen LiObstetrics and Gynecology Department, Xinqiao Hospital, Third Military Medical University, Chongqing 400037, P.R. China.
Lan LiObstetrics and Gynecology Department, Chong Qing Health Center for Women and Children, Chongqing 400010, P.R. China.
Zhengqiong ChenObstetrics and Gynecology Department, Xinqiao Hospital, Third Military Medical University, Chongqing 400037, P.R. China.
Ying YangObstetrics and Gynecology Department, Xinqiao Hospital, Third Military Medical University, Chongqing 400037, P.R. China.
Army Medical University · CNXinqiao Hospital · CNChongqing Maternal and Child Health Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Previous antitumor angiogenesis strategies have focused on targeting angiogenic signals. Encouragingly, the metabolism of tumor endothelial cells (TECs) has gained attention as a therapeutic target in recent years. There is consensus that, in terms of antitumor angiogenesis, the promotion of tumor vascular regression and normalization of the remaining blood vessels are equally important. Presently, tumor vessel normalization (TVN) is an emerging antitumor treatment. The present study focused on the normalization of TEC metabolism. The results demonstrated that TECs have a hyperglycolytic metabolism. Parixibox, a cyclooxygenase‑2 (COX‑2) blocker, successively reduces the expression of vascular endothelial growth factor (VEGF) in the tumor microenvironment. VEGF further influences the expression of 6‑Phosphofructo-2-Kinase/Fructose-2,6‑Biphosphatase 3, a key glycolysis gene. Pharmacological blockade of COX‑2 restored the glucose metabolism level (particularly glycolysis) in TECs, which may be an important basic process in TVN. Therefore, COX‑2, which acts on abnormal tumor vessels, is expected to become a novel target for tumor treatment.

Indexed as

AnimalsAntineoplastic AgentsCyclooxygenase 2Cyclooxygenase 2 InhibitorsDisease ProgressionEndothelial CellsFemaleGlucoseGlycolysisIsoxazolesMice, Inbred C57BLNeoplasmsOvarian NeoplasmsTumor MicroenvironmentVascular Endothelial Growth Factor AAntineoplastic AgentsCyclooxygenase 2Cyclooxygenase 2 InhibitorsGlucoseIsoxazolesparecoxibVascular Endothelial Growth Factor A

Identifiers

PMID29257333
PMCPMC5783508
OpenAlexW2772887932

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.