Evidence map›Paper›PMID 24583467›Full record

ArticleCell cycle (Georgetown, Tex.)2014

Nuclear accumulation of cyclin D1 following long-term fractionated exposures to low-dose ionizing radiation in normal human diploid cells.

Tsutomu Shimura, Nobuyuki Hamada, Megumi Sasatani, Kenji Kamiya, Naoki Kunugita

Abstract read
In one paragraph

Article in Cell cycle (Georgetown, Tex.), 2014. 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
–field-weighted citation impact
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.

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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

5 authors.

Tsutomu ShimuraDepartment of Environmental Health; National Institute of Public Health; Wako, Saitama, Japan.
Nobuyuki HamadaRadiation Safety Research Center; Nuclear Technology Research Laboratory; Central Research Institute of Electric Power Industry (CRIEPI); Tokyo, Japan.
Megumi SasataniDepartment of Experimental Oncology; Research Center for Radiation Genome Medicine; Research Institute for Radiation Biology and Medicine (RIRBM); Hiroshima University; Hiroshima, Japan.
Kenji KamiyaDepartment of Experimental Oncology; Research Center for Radiation Genome Medicine; Research Institute for Radiation Biology and Medicine (RIRBM); Hiroshima University; Hiroshima, Japan.
Naoki KunugitaDepartment of Environmental Health; National Institute of Public Health; Wako, Saitama, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cyclin D1 is a mitogenic sensor that responds to growth signals from the extracellular environment and regulates the G 1-to-S cell cycle transition. When cells are acutely irradiated with a single dose of 10 Gy, cyclin D1 is degraded, causing cell cycle arrest at the G 1/S checkpoint. In contrast, cyclin D1 accumulates in human tumor cells that are exposed to long-term fractionated radiation (0.5 Gy/fraction of X-rays). In this study we investigated the effect of fractionated low-dose radiation exposure on cyclin D1 localization in 3 strains of normal human fibroblasts. To specifically examine the nuclear accumulation of cyclin D1, cells were treated with a hypotonic buffer containing detergent to remove cytoplasmic cyclin D1. Proliferating cell nuclear antigen (PCNA) immunofluorescence was used to identify cells in S phase. With this approach, we observed S-phase nuclear retention of cyclin D1 following low-dose fractionated exposures, and found that cyclin D1 nuclear retention increased with exposure time. Cells that retained nuclear cyclin D1 were more likely to have micronuclei than non-retaining cells, indicating that the accumulation of nuclear cyclin D1 was associated with genomic instability. Moreover, inhibition of the v-akt murine thymoma viral oncogene homolog (AKT) pathway facilitated cyclin D1 degradation and eliminated cyclin D1 nuclear retention in cells exposed to fractionated radiation. Thus, cyclin D1 may represent a useful marker for monitoring long-term effects associated with exposure to low levels of radiation.

Indexed as

BuffersCell NucleusCells, CulturedCyclin DDiploidyDose-Response Relationship, RadiationFibroblastsHumansOncogene Protein v-aktProliferating Cell Nuclear AntigenS Phase Cell Cycle CheckpointsBuffersCyclin DOncogene Protein v-aktProliferating Cell Nuclear AntigenAKTCyclin D1double-strand breakslong-term exposurelow-dose radiation

Identifiers

PMID24583467
PMCPMC4049961

What OpenQuestion holds

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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.