Evidence map›Paper›PMID 12917629›Full record

ArticleOncogene2003

Overexpression of ErbB2 enhances ethanol-stimulated intracellular signaling and invasion of human mammary epithelial and breast cancer cells in vitro.

Cuiling Ma, Hong Lin, Stephen S Leonard, Xianglin Shi, Jianping Ye, Jia Luo

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.4field-weighted citation impact, top 21% 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

24 citing papers in PubMed, 51 citations in OpenAlex.

  1. Alcohol and breast cancer.Pharmacological reports : PR · 2023
    Review
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  15. Ethanol disrupts vascular endothelial barrier: implication in cancer metastasis.Toxicological sciences : an official journal of the Society of Toxicology · 2012
    Article
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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

6 authors at 3 institutions in 1 country.

Cuiling MaDepartment of Microbiology, Immunology and Cell Biology, West Virginia University School of Medicine, Morgantown, WV 26506, USA.
Hong Lin
Stephen S Leonard
Xianglin Shi
Jianping Ye
Jia Luo
West Virginia University · USNational Institute for Occupational Safety and Health · USPennington Biomedical Research Center · US

Funding

ETHANOL, ERBB RECEPTORS AND BREAST CANCERR01CA090385 · NCI · WEST VIRGINIA UNIVERSITY · PI LUO, JIA · 2000 to 2004
$669k
ETHANOL-INDUCED CELL CYCLE DAMAGER03AA012968 · NIAAA · WEST VIRGINIA UNIVERSITY · PI LUO, JIA · 2000 to 2001
$146k
NCI NIH HHS CA90385NIAAA NIH HHS AA12968
6 · The paper itself

Abstract

Both epidemiological and experimental studies indicate that ethanol is a tumor promoter and may promote metastasis of breast cancer. However, the molecular mechanisms underlying ethanol-mediated tumor promotion remain unknown. Overexpression of ErbB proteins in breast cancer patients is generally associated with poor prognosis. The ErbB proteins are a family of receptor kinases that include four closely related members: epidermal growth factor receptor (EGFR/ErbB1), ErbB2/neu, ErbB3, and ErbB4. Particularly, ErbB2 plays a pivotal role in ErbB-mediated activities. Here we demonstrated that amplification of ErbB2 expression sensitized a specific cellular response to ethanol. Human breast cancer cells or mammary epithelial cells with a high expression of ErbB2 exhibited an enhanced response to ethanol-stimulated cell invasion in vitro. Ethanol also stimulated cell proliferation; however, this stimulation was independent of ErbB2 levels. Ethanol triggered divergent intracellular signaling among cells expressing different ErbB2 levels. In the cells overexpressing ErbB2, ethanol was more effective in the activation of c-Jun NH2 terminal protein kinases (JNKs) and p38 mitogen-activated protein kinase (p38 MAPK) as well as the induction of reactive oxygen species (ROS) than the cells with normal ErbB2 expression. Blockage of either JNKs or p38 MAPK activation eliminated ethanol-mediated cell invasion. In contrast, the reduction of hydrogen peroxide concentration by catalase exposure had little effect on ethanol-induced cell invasion. These results indicated that ethanol-induced cell invasion was primarily mediated by JNKs and p38 MAPK, whereas the involvement of ROS formation might be minimal. Our study suggests that overexpression of ErbB2 may augment ethanol-elicited signaling and promote ethanol-stimulated tumor metastasis.

Indexed as

BreastBreast NeoplasmsCentral Nervous System DepressantsErb-b2 Receptor Tyrosine KinasesEthanolFemaleHumansJNK Mitogen-Activated Protein KinasesMitogen-Activated Protein KinasesNeoplasm Invasivenessp38 Mitogen-Activated Protein KinasesReactive Oxygen SpeciesSignal TransductionCentral Nervous System DepressantsErb-b2 Receptor Tyrosine KinasesEthanolJNK Mitogen-Activated Protein KinasesMitogen-Activated Protein Kinasesp38 Mitogen-Activated Protein KinasesReactive Oxygen Species

Identifiers

PMID12917629
OpenAlexW2026566270

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.