Evidence map›Paper›PMID 27959387›Full record

ArticleInternational journal of oncology2017

Long-term exposure of MCF-7 breast cancer cells to ethanol stimulates oncogenic features.

Robert Gelfand, Dolores Vernet, Kevin W Bruhn, Suren Sarkissyan, David Heber, Jaydutt V Vadgama, Nestor F Gonzalez-Cadavid

Open access · hybridAbstract read
In one paragraph

Article in International journal of oncology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
0.9field-weighted citation impact, top 26% 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

13 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Novel Diagnostic Biomarkers in Colorectal Cancer.International journal of molecular sciences · 2022
    Review
  5. Article
  6. Review
  7. 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

7 authors at 2 institutions in 1 country.

Robert GelfandDepartment of Medicine, Charles R. Drew University of Medicine and Science, Los Angeles, CA 90059, USA.
Dolores VernetDepartment of Medicine, Charles R. Drew University of Medicine and Science, Los Angeles, CA 90059, USA.
Kevin W BruhnDavid Geffen School of Medicine at UCLA, Los Angeles, CA 90095, USA.
Suren SarkissyanDepartment of Medicine, Charles R. Drew University of Medicine and Science, Los Angeles, CA 90059, USA.
David HeberDepartment of Medicine and Human Nutrition, David Geffen School of Medicine at UCLA, Los Angeles, CA 90095, USA.
Jaydutt V VadgamaDepartment of Medicine, Charles R. Drew University of Medicine and Science, Los Angeles, CA 90059, USA.
Nestor F Gonzalez-CadavidDepartment of Medicine, Charles R. Drew University of Medicine and Science, Los Angeles, CA 90059, USA.
Charles R. Drew University of Medicine and Science · USUniversity of California, Los Angeles · US

Funding

Training and Mentoring ProgramsU54CA143930 · NCI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI PIETRAS, RICHARD JOSEPH · 2009 to 2020
$7.5M
NCI NIH HHS U54 CA143930
6 · The paper itself

Abstract

Alcohol consumption is a risk factor for breast cancer. Little is known regarding the mechanism, although it is assumed that acetaldehyde or estrogen mediated pathways play a role. We previously showed that long-term exposure to 2.5 mM ethanol (blood alcohol ~0.012%) of MCF-12A, a human normal epithelial breast cell line, induced epithelial mesenchymal transition (EMT) and oncogenic transformation. In this study, we investigated in the human breast cancer cell line MCF-7, whether a similar exposure to ethanol at concentrations ranging up to peak blood levels in heavy drinkers would increase malignant progression. Short-term (1-week) incubation to ethanol at as low as 1-5 mM (corresponding to blood alcohol concentration of ~0.0048-0.024%) upregulated the stem cell related proteins Oct4 and Nanog, but they were reduced after exposure at 25 mM. Long-term (4-week) exposure to 25 mM ethanol upregulated the Oct4 and Nanog proteins, as well as the malignancy marker Ceacam6. DNA microarray analysis in cells exposed for 1 week showed upregulated expression of metallothionein genes, particularly MT1X. Long-term exposure upregulated expression of some malignancy related genes (STEAP4, SERPINA3, SAMD9, GDF15, KRT15, ITGB6, TP63, and PGR, as well as the CEACAM, interferon related, and HLA gene families). Some of these findings were validated by RT-PCR. A similar treatment also modulated numerous microRNAs (miRs) including one regulator of Oct4 as well as miRs involved in oncogenesis and/or malignancy, with only a few estrogen-induced miRs. Long-term 25 mM ethanol also induced a 5.6-fold upregulation of anchorage-independent growth, an indicator of malignant-like features. Exposure to acetaldehyde resulted in little or no effect comparable to that of ethanol. The previously shown alcohol induction of oncogenic transformation of normal breast cells is now complemented by the current results suggesting alcohol's potential involvement in malignant progression of breast cancer.

Indexed as

AcetaldehydeBreast NeoplasmsCarcinogenesisCell ProliferationEpithelial-Mesenchymal TransitionEstrogensEthanolFemaleGene Expression Regulation, NeoplasticHumansMCF-7 CellsMetabolic Networks and PathwaysNeoplasm ProteinsAcetaldehydeEstrogensEthanolNeoplasm Proteins

Identifiers

PMID27959387
PMCPMC5182011
OpenAlexW2559848236

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.