Evidence map›Paper›PMID 12592377›Full record

ArticleBritish journal of cancer2003

Gelsolin suppresses tumorigenicity through inhibiting PKC activation in a human lung cancer cell line, PC10.

N Sagawa, H Fujita, Y Banno, Y Nozawa, H Katoh, N Kuzumaki

Open access · hybridAbstract read
In one paragraph

Article in British journal of cancer, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.5field-weighted citation impact, top 12% 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

17 citing papers in PubMed, 57 citations in OpenAlex.

  1. Review
  2. Article
  3. Secretome profiling ofFrontiers in oncology · 2023
    Article
  4. Review
  5. Differential expression ofEXCLI journal · 2020
    Article
  6. Article
  7. Article
  8. Gelsolin promotes cell growth and invasion through the upregulation of p-AKT and p-P38 pathway in osteosarcoma.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Article
  9. Article
  10. Article
  11. Review
  12. Resveratrol amplifies profibrogenic effects of free fatty acids on human hepatic stellate cells.Hepatology research : the official journal of the Japan Society of Hepatology · 2009
    Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. 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

6 authors at 3 institutions in 1 country.

N SagawaDivision of Cancer Gene Regulation, Research Section of Disease Control, Institute for Genetic Medicine, Hokkaido University, Sapporo, Japan.
H Fujita
Y Banno
Y Nozawa
H Katoh
N Kuzumaki
Hokkaido University · JPGifu University · JPInstitute of Applied Biochemistry · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Gelsolin expression is frequently downregulated in lung cancer and several types of different human cancers. To examine the effects of gelsolin restoration on tumorigenicity, we here stably expressed various levels of gelsolin via gene transfer in lung cancer cells (squamous cell carcinoma line, PC10). We observed the alterations in tumorigenicity in vivo when implanted in nude mice, and the changes in growth properties in vitro. As compared to parental cells and control clones, gelsolin transfectants highly reduced tumorigenicity and repressed cell proliferation. Moreover, we investigated bradykinin-induced responses in gelsolin-overexpressing clones, because agonist-stimulated activation of the phospholipases C (PLC)/protein kinase C (PKC) signal transduction pathway is critical for cell growth and tumorigenicity. Bradykinin promotes phosphatidylinositol 4,5-bisphosphate (PIP2) hydrolysis by PLC and translocation of various PKC isoforms from the cytosolic fraction to the particulate fraction. Bradykinin treatment did not increase inositoltriphosphate (IP3) production and induce the membrane fractions of PKC alpha and PKC gamma in gelsolin tranfectants, while it induced PIP2 hydrolysis and increased the fractions in parental and control clones. These results suggest that gelsolin suppressed the activation of PKCs involved in phospholipid signalling pathways, inhibiting cell proliferation and tumorigenicity.

Indexed as

AnimalsApoptosisBradykininCell DivisionEnzyme ActivationGelsolinHumansInositol 1,4,5-TrisphosphateIsoenzymesLung NeoplasmsMiceMice, NudeModels, BiologicalNeoplasm TransplantationProtein Kinase CProtein TransportBradykininGelsolinInositol 1,4,5-TrisphosphateIsoenzymesProtein Kinase C

Identifiers

PMID12592377
PMCPMC2377162
OpenAlexW2019482305

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.