Evidence map›Paper›PMID 22331491›Full record

ArticleToxicological sciences : an official journal of the Society of Toxicology2012

Ethanol disrupts vascular endothelial barrier: implication in cancer metastasis.

Mei Xu, Gang Chen, Wei Fu, Mingjun Liao, Jacqueline A Frank, Kimberly A Bower, Shengyun Fang, Zhuo Zhang, Xianglin Shi, Jia Luo

Open access · bronzeAbstract read
In one paragraph

Article in Toxicological sciences : an official journal of the Society of Toxicology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.9field-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

20 citing papers in PubMed, 33 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Alcohol and breast cancer.Pharmacological reports : PR · 2023
    Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Ethanol-induced lymphatic endothelial cell permeability via MAP-kinase regulation.American journal of physiology. Cell physiology · 2021
    Article
  12. Review
  13. Article
  14. Article
  15. Review
  16. Review
  17. Article
  18. Article
  19. Review
  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

10 authors at 3 institutions in 1 country.

Mei XuDepartment of Internal Medicine, College of Medicine, University of Kentucky, Lexington, Kentucky 40536, USA.
Gang Chen
Wei Fu
Mingjun Liao
Jacqueline A Frank
Kimberly A Bower
Shengyun Fang
Zhuo Zhang
Xianglin Shi
Jia Luo
University of Kentucky · USUniversity of Maryland, Baltimore · USWest Virginia University · US

Funding

GSK3BETA, A MEDIATOR OF ETHANOL NEUROTOXICITYR01AA015407 · NIAAA · WEST VIRGINIA UNIVERSITY · PI JIA LUO · 2005 to 2026
$6.2M
ALCOHOL AND BREAST CANCERR01AA017226 · NIAAA · WEST VIRGINIA UNIVERSITY · PI LUO, JIA · 2008 to 2024
$5.2M
NIAAA NIH HHS AA017226NIAAA NIH HHS R01 AA015407
6 · The paper itself

Abstract

Both epidemiological and experimental studies indicate that ethanol exposure enhances tumor progression. Ethanol exposure promotes cancer cell invasion and is implicated in tumor metastasis. Metastasis consists of multiple processes involving intravasation and extravasation of cancer cells across the blood vessel walls. The integrity of the vascular endothelial barrier that lines the inner surface of blood vessels plays a critical role in cancer cell intravasation/extravasation. We examined the effects of ethanol on the endothelial integrity in vitro. Ethanol at physiologically relevant concentrations did not alter cell viability but disrupted the endothelial monolayer integrity, which was evident by a decrease in the electric resistance and the appearance of intercellular gaps in the endothelial monolayer. The effect of ethanol was reversible once ethanol was removed. The disruption of the endothelial monolayer integrity was associated with an increased invasion of cancer cells through the endothelial monolayer. Ethanol induced the formation of stress fibers; stabilization of actin filaments by jasplakinolide prevented ethanol-induced disruption of endothelial integrity and cancer cell invasion. VE-cadherin is a critical component of the adherens junctions, which regulates vascular endothelial integrity. Ethanol induced the endocytosis of VE-cadherin and the effect was blocked by jasplakinolide. Our results indicate that ethanol may facilitate cancer metastasis by disrupting the vascular endothelial barrier.

Indexed as

ActinsAntineoplastic AgentsCadherinsCell MovementCell SurvivalCentral Nervous System DepressantsDepsipeptidesDisease ProgressionElectric ImpedanceEndocytosisEthanolGap JunctionsHumansHuman Umbilical Vein Endothelial CellsNeoplasm InvasivenessNeoplasm MetastasisActinsAntineoplastic AgentsCadherinsCentral Nervous System DepressantsDepsipeptidesEthanoljasplakinolide

Identifiers

PMID22331491
PMCPMC3327869
OpenAlexW2152851092

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.