Evidence map›Paper›PMID 35773310›Full record

ArticleScientific reports2022

N(6)-methyladenosine methylation-regulated polo-like kinase 1 cell cycle homeostasis as a potential target of radiotherapy in pancreatic adenocarcinoma.

Shotaro Tatekawa, Keisuke Tamari, Ryota Chijimatsu, Masamitsu Konno, Daisuke Motooka, Suguru Mitsufuji, Hirofumi Akita, Shogo Kobayashi, Yoshiki Murakumo, Yuichiro Doki and 3 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2022. 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
2.3field-weighted citation impact, top 11% 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, 29 citations in OpenAlex.

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  13. The footprint of gut microbiota in gallbladder cancer: a mechanistic review.Frontiers in cellular and infection microbiology · 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

13 authors at 2 institutions in 1 country.

Shotaro TatekawaDepartment of Radiation Oncology, Osaka University Graduate School of Medicine, Yamadaoka 2-2, Suita, Osaka, 565-0871, Japan.
Keisuke TamariDepartment of Radiation Oncology, Osaka University Graduate School of Medicine, Yamadaoka 2-2, Suita, Osaka, 565-0871, Japan.
Ryota ChijimatsuDepartment of Medical Data Science, Center of Medical Innovation and Translational Research, Osaka University Graduate School of Medicine, Yamadaoka 2-2, Suita, Osaka, 565-0871, Japan.
Masamitsu KonnoDepartment of Medical Data Science, Center of Medical Innovation and Translational Research, Osaka University Graduate School of Medicine, Yamadaoka 2-2, Suita, Osaka, 565-0871, Japan.
Daisuke MotookaGenome Information Research Center, Research Institute for Microbial Diseases, Osaka University, Suita, Osaka, 565-0871, Japan.
Suguru MitsufujiDepartment of Gastroenterological Surgery, Osaka University Graduate School of Medicine, Suita, Osaka, 565-0871, Japan.
Hirofumi AkitaDepartment of Gastroenterological Surgery, Osaka University Graduate School of Medicine, Suita, Osaka, 565-0871, Japan.
Shogo KobayashiDepartment of Gastroenterological Surgery, Osaka University Graduate School of Medicine, Suita, Osaka, 565-0871, Japan.
Yoshiki MurakumoDepartment of Pathology, Kitasato University School of Medicine, Sagamihara, Kanagawa, 252-0374, Japan.
Yuichiro DokiDepartment of Gastroenterological Surgery, Osaka University Graduate School of Medicine, Suita, Osaka, 565-0871, Japan.
Hidetoshi EguchiDepartment of Gastroenterological Surgery, Osaka University Graduate School of Medicine, Suita, Osaka, 565-0871, Japan.
Hideshi IshiiDepartment of Medical Data Science, Center of Medical Innovation and Translational Research, Osaka University Graduate School of Medicine, Yamadaoka 2-2, Suita, Osaka, 565-0871, Japan. hishii@gesurg.med.osaka-u.ac.jp.
Kazuhiko OgawaDepartment of Radiation Oncology, Osaka University Graduate School of Medicine, Yamadaoka 2-2, Suita, Osaka, 565-0871, Japan. kogawa@radonc.med.osaka-u.ac.jp.
Osaka University · JPKitasato University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In pancreatic cancer, methyltransferase-like 3 (METTL3), a N(6)-methyladenosine (m6A) methyltransferase, has a favorable effect on tumors and is a risk factor for patients' prognosis. However, the details of what genes are regulated by METTL3 remain unknown. Several RNAs are methylated, and what genes are favored in pancreatic cancer remains unclear. By epitranscriptomic analysis, we report that polo-like kinase 1 (PLK1) is an important hub gene defining patient prognosis in pancreatic cancer and that RNA methylation is involved in regulating its cell cycle-specific expression. We found that insulin like growth factor 2 mRNA binding protein 2 (IGF2BP2) binds to m6A of PLK1 3' untranslated region and is involved in upregulating PLK1 expression and that demethylation of this site activates the ataxia telangiectasia and Rad3-related protein pathway by replicating stress and increasing mitotic catastrophe, resulting in increased radiosensitivity. This suggests that PLK1 methylation is essential for cell cycle maintenance in pancreatic cancer and is a new therapeutic target.

Indexed as

AdenocarcinomaAdenosineCell Cycle ProteinsPancreatic NeoplasmsProtein Serine-Threonine KinasesProto-Oncogene ProteinsCell CycleHomeostasisHumansMethylationMethyltransferasesPolo-Like Kinase 1RNA-Binding ProteinsAdenosineCell Cycle ProteinsIGF2BP2 protein, humanMethyltransferasesMETTL3 protein, humanN-methyladenosinePolo-Like Kinase 1Protein Serine-Threonine KinasesProto-Oncogene ProteinsRNA-Binding Proteins

Identifiers

PMID35773310
PMCPMC9246847
OpenAlexW4283723327

What OpenQuestion holds

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LicenceCC BY
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.