Evidence map›Paper›PMID 26402517›Full record

ArticleCell death & disease2015

DEC1 regulates breast cancer cell proliferation by stabilizing cyclin E protein and delays the progression of cell cycle S phase.

H Bi, S Li, X Qu, M Wang, X Bai, Z Xu, X Ao, Z Jia, X Jiang, Y Yang and 1 more

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2015. 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
2.9field-weighted citation impact, top 9% 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, 67 citations in OpenAlex.

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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 1 country.

H BiSchool of Life Science and Biotechnology, Dalian University of Technology, Dalian 116024, China.
S LiSchool of Life Science and Biotechnology, Dalian University of Technology, Dalian 116024, China.
X QuSchool of Life Science and Medicine, Dalian University of Technology, Panjin 124221, China.
M WangSchool of Life Science and Biotechnology, Dalian University of Technology, Dalian 116024, China.
X BaiSchool of Life Science and Biotechnology, Dalian University of Technology, Dalian 116024, China.
Z XuSchool of Life Science and Biotechnology, Dalian University of Technology, Dalian 116024, China.
X AoSchool of Life Science and Biotechnology, Dalian University of Technology, Dalian 116024, China.
Z JiaSchool of Life Science and Biotechnology, Dalian University of Technology, Dalian 116024, China.
X JiangSchool of Life Science and Biotechnology, Dalian University of Technology, Dalian 116024, China.
Y YangSchool of Life Science and Biotechnology, Dalian University of Technology, Dalian 116024, China.
H WuSchool of Life Science and Biotechnology, Dalian University of Technology, Dalian 116024, China.
Dalian University of Technology · CNDalian University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Breast cancer that is accompanied by a high level of cyclin E expression usually exhibits poor prognosis and clinical outcome. Several factors are known to regulate the level of cyclin E during the cell cycle progression. The transcription factor DEC1 (also known as STRA13 and SHARP2) plays an important role in cell proliferation and apoptosis. Nevertheless, the mechanism of its role in cell proliferation is poorly understood. In this study, using the breast cancer cell lines MCF-7 and T47D, we showed that DEC1 could inhibit the cell cycle progression of breast cancer cells independently of its transcriptional activity. The cell cycle-dependent timing of DEC1 overexpression could affect the progression of the cell cycle through regulating the level of cyclin E protein. DEC1 stabilized cyclin E at the protein level by interacting with cyclin E. Overexpression of DEC1 repressed the interaction between cyclin E and its E3 ligase Fbw7α, consequently reducing the level of polyunbiquitinated cyclin E and increased the accumulation of non-ubiquitinated cyclin E. Furthermore, DEC1 also promoted the nuclear accumulation of Cdk2 and the formation of cyclin E/Cdk2 complex, as well as upregulating the activity of the cyclin E/Cdk2 complex, which inhibited the subsequent association of cyclin A with Cdk2. This had the effect of prolonging the S phase and suppressing the growth of breast cancers in a mouse xenograft model. These events probably constitute the essential steps in DEC1-regulated cell proliferation, thus opening up the possibility of a protein-based molecular strategy for eliminating cancer cells that manifest a high-level expression of cyclin E.

Indexed as

AnimalsBasic Helix-Loop-Helix ProteinsBreast NeoplasmsCell CycleCell ProliferationCyclin EFemaleHomeodomain ProteinsHumansMaleMiceMice, Inbred BALB CMice, NudeOncogene ProteinsS PhaseTransfectionBasic Helix-Loop-Helix ProteinsBhlhe40 protein, mouseCCNE1 protein, humanCyclin EHomeodomain ProteinsOncogene Proteins

Identifiers

PMID26402517
PMCPMC4650443
OpenAlexW2210270878

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.