Evidence map›Paper›PMID 17217624›Full record

ArticleNeoplasia (New York, N.Y.)2006

Expression and effect of inhibition of the ubiquitin-conjugating enzyme E2C on esophageal adenocarcinoma.

Jules Lin, Duna A Raoof, Zhuwen Wang, Mu-Yen Lin, Dafydd G Thomas, Joel K Greenson, Thomas J Giordano, Mark B Orringer, Andrew C Chang, David G Beer and 1 more

Open access · goldAbstract readComparative Study
In one paragraph

Article in Neoplasia (New York, N.Y.), 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
1.2field-weighted citation impact, top 24% 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

41 citing papers in PubMed, 61 citations in OpenAlex.

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  18. Ubiquitin proteasome system research in gastrointestinal cancer.World journal of gastrointestinal oncology · 2016
    Review
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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

11 authors at 2 institutions in 2 countries.

Jules LinSection of General Thoracic Surgery, Department of Surgery, University of Michigan Medical School, Ann Arbor, MI 48109, USA.
Duna A Raoof
Zhuwen Wang
Mu-Yen Lin
Dafydd G Thomas
Joel K Greenson
Thomas J Giordano
Mark B Orringer
Andrew C Chang
David G Beer
Lin Lin
University of Michigan–Ann Arbor · USNational Cheng Kung University · TW

Funding

XenograftP30CA046592 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Scott Michael Schuetze · 1988 to 2026
$178.2M
University of Michigan Surgical Oncology Research Training ProgramT32CA009672 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI JACQUELINE SARA JERUSS, WEIPING ZOU · 1991 to 2026
$6.0M
MOLECULAR STUDIES OF ESOPHAGEAL ADENOCARCINOMAR01CA071606 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI BEER, DAVID GEORGE · 1997 to 2009
$3.1M
NCI NIH HHS 5 P30 CA46592NCI NIH HHS CA71606NCI NIH HHS P30 CA046592NCI NIH HHS R01 CA071606NCI NIH HHS T32 CA009672NCI NIH HHS T32 CA009672-15
6 · The paper itself

Abstract

Ubiquitin-dependent proteolysis of cyclins plays a critical role in cell cycle progression and tumorigenesis. We examined the expression of ubiquitin-conjugating enzyme E2C (UBE2C) during progression from Barrett's metaplasia to esophageal adenocarcinoma (EA) and the effects of targeting this enzyme on EA-derived cell lines. Using oligonucleotide microarrays UBE2C expression was elevated in 73% (11 of 15) of EAs relative to Barrett's metaplasia. Tissue microarray showed elevated UBE2C in 70% (7 of 10) of dysplastic samples and in 87% (58 of 67) of tumors relative to metaplastic samples. Transfection of dominant-negative UBE2C into Seg-1 cells decreased proliferation (P = .04) and increased mitotic arrest compared to vector controls (63.5% vs 6.8%; P < .001). Transfection of UBE2C small interfering RNA also caused inhibiton of cell proliferation and distortion of the cell cycle, with maximal increase of G(2) cells (155% of mock cells) at 72 hours and of S-phase cells (308% of mock cells) at 24 hours. Treatment of Seg-1 cells with the proteasome inhibitor MG-262 (1 nM-1 microM) showed decreased proliferation (P = .02). EA-derived cells expressing UBE2C are sensitive to treatment with MG-262 and to silencing of UBE2C, suggesting that patients with EAs overexpressing UBE2C may benefit from agents targeting this ubiquitin-conjugating enzyme.

Indexed as

Gene Expression Regulation, NeoplasticAdenocarcinomaBoronic AcidsEsophageal NeoplasmsGene Expression Regulation, EnzymologicGrowth InhibitorsHumansMitosisProtease InhibitorsTransfectionTumor Cells, CulturedUbiquitin-Conjugating EnzymesBoronic AcidsGrowth InhibitorsMG 262Protease InhibitorsUBE2C protein, humanUbiquitin-Conjugating Enzymes

Identifiers

PMID17217624
PMCPMC1783715
OpenAlexW1972471610

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.