Evidence map›Paper›PMID 23645673›Full record

ArticleThe Journal of biological chemistry2013

Selective enhancing effect of early mitotic inhibitor 1 (Emi1) depletion on the sensitivity of doxorubicin or X-ray treatment in human cancer cells.

Natsumi Shimizu, Nakako Izumi Nakajima, Takaaki Tsunematsu, Ikuko Ogawa, Hidehiko Kawai, Ryoichi Hirayama, Akira Fujimori, Akiko Yamada, Ryuichi Okayasu, Naozumi Ishimaru and 2 more

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2013. 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
0.8field-weighted citation impact, top 30% 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, 19 citations in OpenAlex.

  1. Article
  2. Article
  3. The role of Fbxo5 in the development of human malignant tumors.American journal of cancer research · 2022
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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

12 authors at 3 institutions in 1 country.

Natsumi ShimizuDepartment of Oral and Maxillofacial Pathobiology, Graduate School of Biomedical & Health Sciences, Hiroshima University, Hiroshima 734-8553, Japan.
Nakako Izumi Nakajima
Takaaki Tsunematsu
Ikuko Ogawa
Hidehiko Kawai
Ryoichi Hirayama
Akira Fujimori
Akiko Yamada
Ryuichi Okayasu
Naozumi Ishimaru
Takashi Takata
Yasusei Kudo
Hiroshima University · JPNational Institutes for Quantum and Radiological Science and Technology · JPTokushima University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chemotherapy and radiation in addition to surgery has proven useful in a number of different cancer types, but the effectiveness in normal tissue cannot be avoided in these therapies. To improve the effectiveness of these therapies selectively in cancer tissue is important for avoiding side effects. Early mitotic inhibitor 1 (Emi1) is known to have the function to inhibit anaphase-promoting complex/cyclosome ubiquitin ligase complex, which ubiquitylates the cell cycle-related proteins. It recently has been shown that Emi1 knockdown prevents transition from S to G2 phase by down-regulating geminin via anaphase-promoting complex/cyclosome activation. At present, anticancer drugs for targeting DNA synthesis to interfere with rapidly dividing cells commonly are used. As Emi1 depletion interferes with completion of DNA synthesis in cancer cells, we thought that Emi1 knockdown might enhance the sensitivity for anticancer agents. Here, we confirmed that Emi1 siRNA induced polyploidy for preventing transition from S to G2 phase in several cancer cell lines. Then, we treated Emi1 depleted cells with doxorubicin. Interestingly, increased apoptotic cells were observed after doxorubicin treatment in Emi1 siRNA-treated cancer cells. In addition, Emi1 depletion enhanced the sensitivity of x-ray irradiation in cancer cells. Importantly, synergistic effect of Emi1 knockdown in these combination therapies was not observed in normal cells. These results suggest that Emi1 siRNA can be a useful tool for enhancing of sensitivity of cancer cells to anticancer reagents and radiation.

Indexed as

Radiation ToleranceAdenomatous Polyposis Coli ProteinAntibiotics, AntineoplasticAntigens, CDApoptosisCadherinsCarcinoma, Squamous CellCdc20 ProteinsCell Cycle ProteinsCell Line, TumorDNA DamageDoxorubicinDrug Resistance, NeoplasmF-Box ProteinsGene ExpressionGene Knockdown TechniquesAdenomatous Polyposis Coli ProteinAntibiotics, AntineoplasticAntigens, CDAPC protein, humanCadherinsCDC20 protein, humanCdc20 ProteinsCDH1 protein, humanCell Cycle ProteinsDoxorubicinF-Box ProteinsFBXO5 protein, humanRNA, Small InterferingAnticancer DrugCancerCancer TherapyCell CycleDNA DamageDNA SynthesisRadiation Biology

Identifiers

PMID23645673
PMCPMC3682528
OpenAlexW1973631495

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.