Evidence map›Paper›PMID 26297435›Full record

ArticleNeoplasia (New York, N.Y.)2015

Dynamic Change in p63 Protein Expression during Implantation of Urothelial Cancer Clusters.

Takahiro Yoshida, Hiroaki Okuyama, Masashi Nakayama, Hiroko Endo, Yasuhiko Tomita, Norio Nonomura, Kazuo Nishimura, Masahiro Inoue

Open access · goldAbstract read
In one paragraph

Article in Neoplasia (New York, N.Y.), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

10 citing papers in PubMed, 14 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. Organoid culture of bladder cancer cells.Investigative and clinical urology · 2018
    Article
  9. Article
  10. 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

8 authors at 2 institutions in 1 country.

Takahiro YoshidaDepartment of Biochemistry, Osaka Medical Center for Cancer and Cardiovascular Diseases; Department of Urology, Osaka University Graduate School of Medicine.
Hiroaki OkuyamaDepartment of Biochemistry, Osaka Medical Center for Cancer and Cardiovascular Diseases.
Masashi NakayamaDepartment of Urology, Osaka Medical Center for Cancer and Cardiovascular Diseases.
Hiroko EndoDepartment of Biochemistry, Osaka Medical Center for Cancer and Cardiovascular Diseases.
Yasuhiko TomitaDepartment of Pathology, Osaka Medical Center for Cancer and Cardiovascular Diseases.
Norio NonomuraDepartment of Urology, Osaka University Graduate School of Medicine.
Kazuo NishimuraDepartment of Urology, Osaka Medical Center for Cancer and Cardiovascular Diseases.
Masahiro InoueDepartment of Biochemistry, Osaka Medical Center for Cancer and Cardiovascular Diseases; Department of Clinical and Experimental Pathophysiology, Osaka University Graduate School of Pharmaceutical Sciences. Electronic address: inoue-ma2@mc.pref.osaka.jp.
Osaka International Cancer Institute · JPThe University of Osaka · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although the dissemination of urothelial cancer cells is supposed to be a major cause of the multicentricity of urothelial tumors, the mechanism of implantation has not been well investigated. Here, we found that cancer cell clusters from the urine of patients with urothelial cancer retain the ability to survive, grow, and adhere. By using cell lines and primary cells collected from multiple patients, we demonstrate that △Np63α protein in cancer cell clusters was rapidly decreased through proteasomal degradation when clusters were attached to the matrix, leading to downregulation of E-cadherin and upregulation of N-cadherin. Decreased △Np63α protein level in urothelial cancer cell clusters was involved in the clearance of the urothelium. Our data provide the first evidence that clusters of urothelial cancer cells exhibit dynamic changes in △Np63α expression during attachment to the matrix, and decreased △Np63α protein plays a critical role in the interaction between cancer cell clusters and the urothelium. Thus, because △Np63α might be involved in the process of intraluminal dissemination of urothelial cancer cells, blocking the degradation of △Np63α could be a target of therapy to prevent the dissemination of urothelial cancer.

Indexed as

Biomarkers, TumorCadherinsCell AdhesionCell ProliferationCell SurvivalEpithelial CellsHumansSignal TransductionSpheroids, CellularTranscription FactorsTumor Cells, CulturedTumor Suppressor ProteinsUrineUrologic NeoplasmsUrotheliumBiomarkers, TumorCadherinsTP63 protein, humanTranscription FactorsTumor Suppressor Proteins

Identifiers

PMID26297435
PMCPMC4547408
OpenAlexW1828956177

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.