Evidence map›Paper›PMID 34659892›Full record

ArticleAmerican journal of cancer research2021

Induction of cellular senescence in fibroblasts through β1-integrin activation by tenascin-C-derived peptide and its protumor effect.

Motomichi Fujita, Manabu Sasada, Mayu Eguchi, Takuya Iyoda, Shin Okuyama, Takuro Osawa, Kenta Tsuzuranuki, Mamoru Sakamoto, Yu Hagihara, Masaki Matsumura and 4 more

Open access · greenAbstract read
In one paragraph

Article in American journal of cancer research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.1field-weighted citation impact, top 25% 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

12 citing papers in PubMed, 10 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Review
  7. Senescence-Associated Alterations in Matrisome of Mesenchymal Stem Cells.International journal of molecular sciences · 2024
    Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. 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

14 authors at 2 institutions in 1 country.

Motomichi FujitaDepartment of Molecular Patho-Physiology, Faculty of Pharmaceutical Sciences, Tokyo University of Science Chiba, Japan.
Manabu SasadaDepartment of Molecular Patho-Physiology, Faculty of Pharmaceutical Sciences, Tokyo University of Science Chiba, Japan.
Mayu EguchiDepartment of Molecular Patho-Physiology, Faculty of Pharmaceutical Sciences, Tokyo University of Science Chiba, Japan.
Takuya IyodaDepartment of Pharmacy, Faculty of Pharmaceutical Sciences, Sanyo-Onoda City University Yamaguchi, Japan.
Shin OkuyamaDepartment of Molecular Patho-Physiology, Faculty of Pharmaceutical Sciences, Tokyo University of Science Chiba, Japan.
Takuro OsawaDepartment of Molecular Patho-Physiology, Faculty of Pharmaceutical Sciences, Tokyo University of Science Chiba, Japan.
Kenta TsuzuranukiDepartment of Molecular Patho-Physiology, Faculty of Pharmaceutical Sciences, Tokyo University of Science Chiba, Japan.
Mamoru SakamotoDepartment of Molecular Patho-Physiology, Faculty of Pharmaceutical Sciences, Tokyo University of Science Chiba, Japan.
Yu HagiharaDepartment of Molecular Patho-Physiology, Faculty of Pharmaceutical Sciences, Tokyo University of Science Chiba, Japan.
Masaki MatsumuraDepartment of Molecular Patho-Physiology, Faculty of Pharmaceutical Sciences, Tokyo University of Science Chiba, Japan.
Satoshi OsadaFaculty of Science and Engineering, Saga University Saga, Japan.
Hiroaki KodamaFaculty of Science and Engineering, Saga University Saga, Japan.
Yoshikazu HigamiLaboratory of Molecular Pathology and Metabolic Disease, Faculty of Pharmaceutical Sciences, Tokyo University of Science Chiba, Japan.
Fumio FukaiDepartment of Molecular Patho-Physiology, Faculty of Pharmaceutical Sciences, Tokyo University of Science Chiba, Japan.
Tokyo University of Science · JPSaga University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tenascin-C is upregulated during inflammation and tumorigenesis, and its expression level is correlated with a poor prognosis in several malignancies. Nevertheless, the substantial role of tenascin-C in cancer progression is poorly understood. Previously, we found that a peptide derived from tenascin-C, termed TNIIIA2, acts directly on tumor cells to activate β1-integrin and induce malignant progression. Here, we show that β1-integrin activation by TNIIIA2 in human fibroblasts indirectly contributes to cancer progression through the induction of cellular senescence. Prolonged treatment of fibroblasts with TNIIIA2 induced cellular senescence, as characterized by the suppression of cell growth and the induction of senescence-associated-β-galactosidase and p16

Indexed as

cancer-associated fibroblastcellular senescenceheparin-binding epidermal growth factor-like growth factorSASPTenascin-Cβ1-integrin

Identifiers

PMID34659892
PMCPMC8493383
OpenAlexW3206349758

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.