Evidence map›Paper›PMID 22301112›Full record

ArticleAmerican journal of physiology. Gastrointestinal and liver physiology2012

The decreased expression of Beclin-1 correlates with progression to esophageal adenocarcinoma: the role of deoxycholic acid.

Heather B Roesly, Mohammad R Khan, Hwu Dau Rw Chen, Kimberly A Hill, Nirushan Narendran, George S Watts, Xiaoxin Chen, Katerina Dvorak

Abstract read
In one paragraph

Article in American journal of physiology. Gastrointestinal and liver physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

35 citing papers in PubMed, 58 citations in OpenAlex.

  1. Article
  2. Review
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  6. Chemosensitization Effect of Seabuckthorn (Foods (Basel, Switzerland) · 2022
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  7. The role of bile acids in carcinogenesis.Cellular and molecular life sciences : CMLS · 2022
    Review
  8. Article
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  11. Alterations in the CaExploration of targeted anti-tumor therapy · 2021
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  14. Article
  15. Review
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  17. Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 2 institutions in 1 country.

Heather B RoeslyDepartment of Cellular and Molecular Medicine, University of Arizona, Tucson, AZ 85724, USA.
Mohammad R Khan
Hwu Dau Rw Chen
Kimberly A Hill
Nirushan Narendran
George S Watts
Xiaoxin Chen
Katerina Dvorak
University of Arizona · USNorth Carolina Central University · US

Funding

VITAMIN AP30CA023074 · NCI · UNIVERSITY OF ARIZONA · PI Dan Theodorescu · 1985 to 2026
$110.2M
SOUTHWEST ENVIRONMENTAL HEALTH SCIENCES CENTERP30ES006694 · NIEHS · UNIVERSITY OF ARIZONA · PI DEAN BILLHEIMER · 1994 to 2026
$36.7M
SPORE in Gastrointestinal CancerP50CA095060 · NCI · UNIVERSITY OF ARIZONA · PI GERNER, EUGENE W · 2002 to 2012
$25.3M
NCI NIH HHS CA-95060NCI NIH HHS P30 CA023074NIEHS NIH HHS P30 ES006694
6 · The paper itself

Abstract

Beclin-1 has a central role in the regulation of autophagy. Barrett's esophagus (BE) is associated with a significantly increased risk for the development of esophageal adenocarcinoma (EAC). In the current study, we evaluated the role of Beclin-1 and autophagy in the EAC. Biopsies obtained from patients with BE and EAC, tissues from a rat model of BE and EAC, and esophageal cell lines were evaluated for the expression of Beclin-1 by immunohistochemistry, immunoblotting, or RT-PCR. Since reflux of bile acids is important in EAC, we also evaluated the effect of exposure to deoxycholic acid (DCA) on autophagy and Beclin-1 expression. Beclin-1 expression was high in squamous epithelium and nondysplastic BE, whereas its expression was low in dysplastic BE and EAC. The same pattern of expression was observed in rat tissues and in esophageal cell lines. Normal esophageal epithelium and HET-1A cells (derived from normal squamous epithelium) show high levels of Beclin-1, but lower levels of Beclin-1 were found in BE and EAC cell lines (CP-A, CP-C, and OE33). Acute exposure to DCA led to increased Beclin-1 expression and increased autophagy as evaluated by electron microscopy and counting percentage of GFP-LC3-positive BE cells with punctate pattern. In contrast, chronic exposure to DCA did not result in the alteration of Beclin-1 levels or autophagy. In summary, these data suggest that autophagy is initially activated in response to bile acids, but chronic exposure to bile acids leads to decreased Beclin-1 expression and autophagy resistance.

Indexed as

AdenocarcinomaAmino AcidsAnimalsApoptosis Regulatory ProteinsAutophagyBarrett EsophagusBeclin-1Bile Acids and SaltsBlotting, WesternCell Line, TumorCell ProliferationDeoxycholic AcidDisease ProgressionEsophageal NeoplasmsHumansImmunohistochemistryAmino AcidsApoptosis Regulatory ProteinsBeclin-1BECN1 protein, humanBile Acids and SaltsDeoxycholic AcidMembrane ProteinsRNARNA, Small Interfering

Identifiers

PMID22301112
PMCPMC3355563
OpenAlexW2165494420

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.