Evidence map›Paper›PMID 35408845›Full record

ArticleInternational journal of molecular sciences2022

PARP Inhibitor Decreases Akt Phosphorylation and Induces Centrosome Amplification and Chromosomal Aneuploidy in CHO-K1 Cells.

Masakazu Tanaka, Masatoshi Mushiake, Jun Takahashi, Yuka Sasaki, Sachiko Yamashita, Chieri Ida, Mitsuko Masutani, Masanao Miwa

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.3field-weighted citation impact, top 43% 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

3 citing papers in PubMed, 3 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
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

8 authors at 4 institutions in 1 country.

Masakazu TanakaDepartment of Microbiology, Kansai Medical University, Osaka 573-1010, Japan.ORCID 0000-0003-4098-385X
Masatoshi MushiakeFaculty of Bioscience, Nagahama Institute of Bio-Science and Technology, Nagahama 526-0829, Japan.
Jun TakahashiFaculty of Bioscience, Nagahama Institute of Bio-Science and Technology, Nagahama 526-0829, Japan.
Yuka SasakiLaboratory of Collaborative Research, Division of Cellular Signaling and Radioisotope Division, National Cancer Center Research Institute, Tokyo 104-0045, Japan.
Sachiko YamashitaFaculty of Bioscience, Nagahama Institute of Bio-Science and Technology, Nagahama 526-0829, Japan.
Chieri IdaDepartment of Applied Life Sciences, College of Nagoya Women's University, Nagoya-shi 467-8610, Japan.
Mitsuko MasutaniLaboratory of Collaborative Research, Division of Cellular Signaling and Radioisotope Division, National Cancer Center Research Institute, Tokyo 104-0045, Japan.
Masanao MiwaFaculty of Bioscience, Nagahama Institute of Bio-Science and Technology, Nagahama 526-0829, Japan.ORCID 0000-0003-4711-7794
Nagahama Institute of Bio-Science and Technology · JPNagasaki University · JPKagoshima University · JPNagoya Women's University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cancer cells are known to have chromosomal number abnormalities (aneuploidy), a hallmark of malignant tumors. Cancer cells also have an increased number of centrosomes (centrosome amplification). Paradoxically, cancer therapies, including γ-irradiation and some anticancer drugs, are carcinogenic and can induce centrosome amplification and chromosomal aneuploidy. Thus, the processes of carcinogenesis and killing cancer cells might have some mechanisms in common. Previously, we found that the inhibitors of polyADP-ribosylation, a post-translational modification of proteins, caused centrosome amplification. However, the mechanism of action of the inhibitors of polyADP-ribosylation is not fully understood. In this study, we found that an inhibitor of polyADP-ribosylation, 3-aminobenzamide, caused centrosome amplification, as well as aneuploidy of chromosomes in CHO-K1 cells. Moreover, inhibitors of polyADP-ribosylation inhibited AKT phosphorylation, and inhibitors of AKT phosphorylation inhibited polyADP-ribosylation, suggesting the involvement of polyADP-ribosylation in the PI3K/Akt/mTOR signaling pathway for controlling cell proliferation. Our data suggest a possibility for developing drugs that induce centrosome amplification and aneuploidy for therapeutic applications to clinical cancer.

Indexed as

Antineoplastic AgentsNeoplasmsAneuploidyAnimalsCentrosomeChromosomal InstabilityChromosomesCricetinaeCricetulusPhosphatidylinositol 3-KinasesPhosphorylationPoly(ADP-ribose) Polymerase InhibitorsProto-Oncogene Proteins c-aktAntineoplastic AgentsPhosphatidylinositol 3-KinasesPoly(ADP-ribose) Polymerase InhibitorsProto-Oncogene Proteins c-aktAktcell proliferationcentrosome amplificationchromosome aneuploidyPARP inhibitorspolyADP-ribosylation

Identifiers

PMID35408845
PMCPMC8998298
OpenAlexW4220892006

What OpenQuestion holds

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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.