Evidence map›Paper›PMID 23170925›Full record

ArticleBMC cancer2012

PTPRZ1 regulates calmodulin phosphorylation and tumor progression in small-cell lung carcinoma.

Hideki Makinoshima, Genichiro Ishii, Motohiro Kojima, Satoshi Fujii, Youichi Higuchi, Takeshi Kuwata, Atsushi Ochiai

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
0.8field-weighted citation impact, top 28% 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

21 citing papers in PubMed, 34 citations in OpenAlex.

  1. Article
  2. Article
  3. CaBiomolecules · 2023
    Review
  4. Article
  5. Article
  6. Review
  7. Overexpression of PTPRZ1 Regulates p120/Journal of oncology · 2022
    Article
  8. Article
  9. The Effect ofFrontiers in pharmacology · 2021
    Review
  10. Article
  11. Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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

7 authors at 2 institutions in 1 country.

Hideki MakinoshimaPathology Division, Research Center for Innovative Oncology, National Cancer Center Hospital East, 6-5-1 Kashiwanoha, Kashiwa, Chiba, 277-8577, Japan.
Genichiro Ishii
Motohiro Kojima
Satoshi Fujii
Youichi Higuchi
Takeshi Kuwata
Atsushi Ochiai
National Cancer Center Hospital East · JPThe University of Tokyo · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundSmall-cell lung carcinoma (SCLC) is a neuroendocrine tumor subtype and comprises approximately 15% of lung cancers. Because SCLC is still a disease with a poor prognosis and limited treatment options, there is an urgent need to develop targeted molecular agents for this disease.

methodsWe screened 20 cell lines from a variety of pathological phenotypes established from different organs by RT-PCR. Paraffin-embedded tissue from 252 primary tumors was examined for PTPRZ1 expression using immunohistochemistry. shRNA mediated PTPRZ1 down-regulation was used to study impact on tyrosine phosphorylation and in vivo tumor progression in SCLC cell lines.

resultsHere we show that PTPRZ1, a member of the protein tyrosine- phosphatase receptor (PTPR) family, is highly expressed in SCLC cell lines and specifically exists in human neuroendocrine tumor (NET) tissues. We also demonstrate that binding of the ligand of PTPRZ1, pleiotrophin (PTN), activates the PTN/PTPRZ1 signaling pathway to induce tyrosine phosphorylation of calmodulin (CaM) in SCLC cells, suggesting that PTPRZ1 is a regulator of tyrosine phosphorylation in SCLC cells. Furthermore, we found that PTPRZ1 actually has an important oncogenic role in tumor progression in the murine xenograft model.

conclusionPTPRZ1 was highly expressed in human NET tissues and PTPRZ1 is an oncogenic tyrosine phosphatase in SCLCs. These results imply that a new signaling pathway involving PTPRZ1 could be a feasible target for treatment of NETs.

Indexed as

AnimalsBlotting, WesternCalmodulinCarcinoma, NeuroendocrineCell Line, TumorDisease Models, AnimalDisease ProgressionHumansImmunohistochemistryLung NeoplasmsMiceMice, SCIDNeoplasm ProteinsPhosphorylationPrognosisReceptor-Like Protein Tyrosine Phosphatases, Class 5CalmodulinNeoplasm ProteinsPTPRZ1 protein, humanReceptor-Like Protein Tyrosine Phosphatases, Class 5Receptor Protein-Tyrosine KinasesRNA, Small Interfering

Identifiers

PMID23170925
PMCPMC3577502
OpenAlexW2092525091

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.