Evidence map›Paper›PMID 38637316›Full record

ArticleJournal of radiation research2024

Sustained activation of the FGF1-MEK-ERK pathway inhibits proliferation, invasion and migration and enhances radiosensitivity in mouse angiosarcoma cells.

Taichi Miura, Junko Kado, Kazuma Ashisuke, Mikio Masuzawa, Fumiaki Nakayama

Open access · goldAbstract read
In one paragraph

Article in Journal of radiation research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact, top 91% 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

1 citing paper in PubMed, 0 citations in OpenAlex.

  1. 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

5 authors at 3 institutions in 2 countries.

Taichi MiuraRegenerative Therapy Research Group, Department of Radiation Regulatory Science Research, National Institute of Radiological Sciences (NIRS), National Institutes for Quantum Science and Technology (QST), 4-9-1 Anagawa, Inage-ku, Chiba 263-8555, Japan.
Junko KadoRegenerative Therapy Research Group, Department of Radiation Regulatory Science Research, National Institute of Radiological Sciences (NIRS), National Institutes for Quantum Science and Technology (QST), 4-9-1 Anagawa, Inage-ku, Chiba 263-8555, Japan.
Kazuma AshisukeRadiation Effect Research Group, Department of Accelerator and Medical Physics, Institute for Quantum Medical Science, National Institutes for Quantum Science and Technology (QST), 4-9-1 Anagawa, Inage-ku, Chiba 263-8555, Japan.
Mikio MasuzawaDepartment of Dermatology, Iwase General Hospital, 20 Kitamachi, Sukagawa-shi, Fukushima 962-8503, Japan.
Fumiaki NakayamaRegenerative Therapy Research Group, Department of Radiation Regulatory Science Research, National Institute of Radiological Sciences (NIRS), National Institutes for Quantum Science and Technology (QST), 4-9-1 Anagawa, Inage-ku, Chiba 263-8555, Japan.
Centre for Innovation in Regulatory Science · GBNational Institutes for Quantum and Radiological Science and Technology · JPRadiation Effects Research Foundation · JP

Funding

JSPS KAKENHI JP18K15571
6 · The paper itself

Abstract

Angiosarcoma is a rare refractory soft-tissue tumor with a poor prognosis and is treated by radiotherapy. The fibroblast growth factor 1 (FGF1) mutant, with enhanced thermostability due to several substituted amino acids, inhibits angiosarcoma cell metastasis, yet the mechanism of action is unclear. This study aims to clarify the FGF1 mutant mechanism of action using ISOS-1 mouse angiosarcoma cells. The wild-type FGF1 or FGF1 mutant was added to ISOS-1 cells and cultured, evaluating cell numbers over time. The invasive and migratory capacity of ISOS-1 cells was assessed by transwell analysis. ISOS-1 cell radiosensitivity was assessed by colony formation assay after X-ray irradiation. To examine whether mitogen-activated protein kinase (MEK) inhibitor counteracts the FGF1 mutant effects, a combination of MEK inhibitor and FGF1 mutant was added to ISOS-1 cells and cultured. The FGF1 mutant was observed to inhibit ISOS-1 cell proliferation, invasion and migration by sustained FGF1 signaling activation. A MEK inhibitor suppressed the FGF1 mutant-induced inhibition of proliferation, invasion and migration of ISOS-1 cells. Furthermore, the FGF1 mutant enhanced radiosensitivity of ISOS-1 cells, but MEK inhibition suppressed the increased radiosensitivity. In addition, we found that the FGF1 mutant strongly inhibits actin polymerization, suggesting that actin cytoskeletal dynamics are closely related to ISOS-1 cell radiosensitivity. Overall, this study demonstrated that in ISOS-1 cells, the FGF1 mutant inhibits proliferation, invasion and migration while enhancing radiosensitivity through sustained activation of the MEK-mediated signaling pathway.

Indexed as

Cell MovementCell ProliferationFibroblast Growth Factor 1HemangiosarcomaMAP Kinase Signaling SystemNeoplasm InvasivenessRadiation ToleranceAnimalsCell Line, TumorMiceFibroblast Growth Factor 1actin polymerizationangiosarcoma cellsFGF1MEK inhibitorradiosensitivity

Identifiers

PMID38637316
PMCPMC11115473
OpenAlexW4394908645

What OpenQuestion holds

Textmetadata
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.