Evidence map›Paper›PMID 29568361›Full record

ArticleOncotarget2018

Colorectal cancer cells require glycogen synthase kinase-3β for sustaining mitosis via translocated promoter region (TPR)-dynein interaction.

Firli R P Dewi, Takahiro Domoto, Masaharu Hazawa, Akiko Kobayashi, Takayuki Douwaki, Toshinari Minamoto, Richard W Wong

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

22 citing papers in PubMed, 32 citations in OpenAlex.

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  6. Advances in the understanding of nuclear pore complexes in human diseases.Journal of cancer research and clinical oncology · 2024
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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

7 authors at 2 institutions in 1 country.

Firli R P DewiFaculty of Natural System, Institute of Natural Science and Technology, Kanazawa University, Kanazawa, Japan.
Takahiro DomotoDivision of Translational and Clinical Oncology, Cancer Research Institute, Kanazawa University, Kanazawa, Japan.
Masaharu HazawaCell-Bionomics Research Unit, Innovative Integrated Bio-Research Core, Institute for Frontier Science Initiative, Kanazawa University, Kanazawa, Japan.
Akiko KobayashiFaculty of Natural System, Institute of Natural Science and Technology, Kanazawa University, Kanazawa, Japan.
Takayuki DouwakiFaculty of Natural System, Institute of Natural Science and Technology, Kanazawa University, Kanazawa, Japan.
Toshinari MinamotoDivision of Translational and Clinical Oncology, Cancer Research Institute, Kanazawa University, Kanazawa, Japan.
Richard W WongFaculty of Natural System, Institute of Natural Science and Technology, Kanazawa University, Kanazawa, Japan.
Kanazawa University · JPLife Science Institute · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glycogen synthase kinase (GSK) 3β, which mediates fundamental cellular signaling pathways, has emerged as a potential therapeutic target for many types of cancer including colorectal cancer (CRC). During mitosis, GSK3β localizes in mitotic spindles and centrosomes, however its function is largely unknown. We previously demonstrated that translocated promoter region (TPR, a nuclear pore component) and dynein (a molecular motor) cooperatively contribute to mitotic spindle formation. Such knowledge encouraged us to investigate putative functional interactions among GSK3β, TPR, and dynein in the mitotic machinery of CRC cells. Here, we show that inhibition of GSK3β attenuated proliferation, induced cell cycle arrest at G2/M phase, and increased apoptosis of CRC cells. Morphologically, GSK3β inhibition disrupted chromosome segregation, mitotic spindle assembly, and centrosome maturation during mitosis, ultimately resulting in mitotic cell death. These changes in CRC cells were associated with decreased expression of TPR and dynein, as well as disruption of their functional colocalization with GSK3β in mitotic spindles and centrosomes. Clinically, we showed that

Indexed as

cell cyclecolon cancerdyneinglycogen synthase kinase-3βtranslocated promoter region (TPR)

Identifiers

PMID29568361
PMCPMC5862582
OpenAlexW2790971434

What OpenQuestion holds

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LicenceCC BY
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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.