Evidence map›Paper›PMID 32214089›Full record

ArticleNature communications2020

CDK1 dependent phosphorylation of hTERT contributes to cancer progression.

Mami Yasukawa, Yoshinari Ando, Taro Yamashita, Yoko Matsuda, Shisako Shoji, Masaki Suimye Morioka, Hideya Kawaji, Kumiko Shiozawa, Mitsuhiro Machitani, Takaya Abe and 9 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

38 citing papers in PubMed, 62 citations in OpenAlex.

  1. Article
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  9. CEP55: Implications for Immunotherapy and Survival in Hepatocellular Carcinoma.Combinatorial chemistry & high throughput screening · 2025
    Article
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  12. Review
  13. Telomeres and telomerase in Sarcoma disease and therapy.International journal of medical sciences · 2024
    Review
  14. Review
  15. Article
  16. Article
  17. Phosphorylation of USP29 by CDK1 Governs TWIST1 Stability and Oncogenic Functions.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023
    Article
  18. Review
  19. Review
  20. Review
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

19 authors at 7 institutions in 3 countries.

Mami Yasukawa *Division of Cancer Stem Cell, National Cancer Center Research Institute, Tokyo, 104-0045, Japan.ORCID http://orcid.org/0000-0002-4214-8922
Yoshinari Ando *Division of Cancer Stem Cell, National Cancer Center Research Institute, Tokyo, 104-0045, Japan.ORCID http://orcid.org/0000-0002-8128-6201
Taro Yamashita *Department of Gastroenterology, Kanazawa University Graduate School of Medical Science, Kanazawa, 920-8641, Japan.ORCID http://orcid.org/0000-0002-3383-9131
Yoko MatsudaDepartment of Pathology, Tokyo Metropolitan Geriatric Hospital and Institute of Gerontology, Tokyo, 173-0015, Japan.
Shisako ShojiLaboratory for Protein Functional and Structural Biology, RIKEN Center for Biosystems Dynamics Research, Yokohama, 230-0045, Japan.ORCID http://orcid.org/0000-0001-8787-2159
Masaki Suimye MoriokaPreventive Medicine and Applied Genomics Unit, RIKEN Center for Integrative Medical Sciences, Yokohama, 230-0045, Japan.
Hideya KawajiPreventive Medicine and Applied Genomics Unit, RIKEN Center for Integrative Medical Sciences, Yokohama, 230-0045, Japan.ORCID http://orcid.org/0000-0002-0575-0308
Kumiko ShiozawaDivision of Rare Cancer Research, National Cancer Center Research Institute, Tokyo, 104-0045, Japan.ORCID http://orcid.org/0000-0002-9173-6798
Mitsuhiro MachitaniDivision of Cancer Stem Cell, National Cancer Center Research Institute, Tokyo, 104-0045, Japan.
Takaya AbeAnimal Resource Development Unit, RIKEN Center for Life Science Technologies, Kobe, 650-0047, Japan.
Shinji YamadaDepartment of Antibody Drug Development, Tohoku University Graduate School of Medicine, Sendai, 980-8575, Japan.ORCID http://orcid.org/0000-0003-4904-7590
Mika K KanekoDepartment of Antibody Drug Development, Tohoku University Graduate School of Medicine, Sendai, 980-8575, Japan.ORCID http://orcid.org/0000-0002-4158-9208
Yukinari KatoDepartment of Antibody Drug Development, Tohoku University Graduate School of Medicine, Sendai, 980-8575, Japan.ORCID http://orcid.org/0000-0001-5385-8201
Yasuhide FurutaAnimal Resource Development Unit, RIKEN Center for Life Science Technologies, Kobe, 650-0047, Japan.
Tadashi KondoDivision of Rare Cancer Research, National Cancer Center Research Institute, Tokyo, 104-0045, Japan.
Mikako ShirouzuLaboratory for Protein Functional and Structural Biology, RIKEN Center for Biosystems Dynamics Research, Yokohama, 230-0045, Japan.ORCID http://orcid.org/0000-0002-7997-2149
Yoshihide HayashizakiRIKEN Preventive Medicine and Diagnosis Innovation Program, Wako, 351-0198, Japan.ORCID http://orcid.org/0000-0002-0561-2802
Shuichi KanekoDepartment of Gastroenterology, Kanazawa University Graduate School of Medical Science, Kanazawa, 920-8641, Japan.ORCID http://orcid.org/0000-0001-7113-3319
Kenkichi MasutomiDivision of Cancer Stem Cell, National Cancer Center Research Institute, Tokyo, 104-0045, Japan. kmasutom@ncc.go.jp.ORCID http://orcid.org/0000-0002-6739-4257
National Cancer Centre Japan · JPTohoku University · JPKanazawa University · JPRIKEN · JPRIKEN Center for Biosystems Dynamics Research · JPKagawa University · JPRIKEN Center for Integrative Medical Sciences · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The telomerase reverse transcriptase is upregulated in the majority of human cancers and contributes directly to cell transformation. Here we report that hTERT is phosphorylated at threonine 249 during mitosis by the serine/threonine kinase CDK1. Clinicopathological analyses reveal that phosphorylation of hTERT at threonine 249 occurs more frequently in aggressive cancers. Using CRISPR/Cas9 genome editing, we introduce substitution mutations at threonine 249 in the endogenous hTERT locus and find that phosphorylation of threonine 249 is necessary for hTERT-mediated RNA dependent RNA polymerase (RdRP) activity but dispensable for reverse transcriptase and terminal transferase activities. Cap Analysis of Gene Expression (CAGE) demonstrates that hTERT phosphorylation at 249 regulates the expression of specific genes that are necessary for cancer cell proliferation and tumor formation. These observations indicate that phosphorylation at threonine 249 regulates hTERT RdRP and contributes to cancer progression in a telomere independent manner.

Indexed as

AnimalsCDC2 Protein KinaseCell Line, TumorCell ProliferationCell Transformation, NeoplasticGene Expression Regulation, NeoplasticHeLa CellsHumansMiceMitosisMutationNeoplasmsPhosphorylationRNA-Dependent RNA PolymeraseTelomeraseThreonineCDC2 Protein KinaseCDK1 protein, humanRNA-Dependent RNA PolymeraseTelomeraseTERT protein, humanThreonine

Identifiers

PMID32214089
PMCPMC7096428
OpenAlexW3014070026

What OpenQuestion holds

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LicenceCC BY
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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.