Evidence map›Paper›PMID 19893046›Full record

ArticleThe American journal of pathology2009

Down-regulation of FXYD3 expression in human lung cancers: its mechanism and potential role in carcinogenesis.

Koji Okudela, Takuya Yazawa, Jun Ishii, Tetsukan Woo, Hideaki Mitsui, Tomoyasu Bunai, Masashi Sakaeda, Hiroaki Shimoyamada, Hanako Sato, Michihiko Tajiri and 4 more

Erratum issuedOpen access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing 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

20 citing papers in PubMed, 39 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Article
  6. Article
  7. Review
  8. FXYD3 facilitates NaAmerican journal of physiology. Cell physiology · 2022
    Article
  9. Cancers · 2022
    Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Expression of HDAC9 in lung cancer--potential role in lung carcinogenesis.International journal of clinical and experimental pathology · 2014
    Article
  19. Article
  20. Article
4 · The record

Corrections and comments

  • Erratum issued
5 · Who and what money

Authors and funding

14 authors at 4 institutions in 1 country.

Koji OkudelaDepartment of Pathology, Yokohama City University Graduate School of Medicine, Kanazawa-Ku, Yokohama, Japan.
Takuya Yazawa
Jun Ishii
Tetsukan Woo
Hideaki Mitsui
Tomoyasu Bunai
Masashi Sakaeda
Hiroaki Shimoyamada
Hanako Sato
Michihiko Tajiri
Nobuo Ogawa
Munetaka Masuda
Haruhiko Sugimura
Hitoshi Kitamura
Yokohama City University · JPKanagawa Cardiovascular and Respiratory Center · JPMinistry of Education, Culture, Sports, Science and Technology · JPHamamatsu University School of Medicine · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

FXYD3 is a FXYD-containing Na,K-ATPase ion channel regulator first identified as a protein overexpressed in murine breast tumors initiated by oncogenic ras or neu. However, our preliminary study revealed that FXYD3 expression was down-regulated in oncogenic KRAS-transduced airway epithelial cells. This contradiction led us to investigate the role of FXYD3 in carcinogenesis of the lung. FXYD3 mRNA and protein levels were lower in most of the lung cancer cell lines than in either the noncancerous lung tissue or airway epithelial cells. Protein levels were also lower in a considerable proportion of primary lung cancers than in nontumoral airway epithelia; FXYD3 expression levels decreased in parallel with the dedifferentiation process. Also, a somatic point mutation, g55c (D19H), was found in one cell line. Forced expression of the wild-type FXYD3, but not the mutant, restored the well-demarcated distribution of cortical actin in cancer cells that had lost FXYD3 expression, suggesting FXYD3 plays a role in the maintenance of cytoskeletal integrity. However, no association between FXYD3 expression and its promoter's methylation status was observed. Therefore, inactivation of FXYD3 through a gene mutation or unknown mechanism could be one cause of the atypical shapes of cancer cells and play a potential role in the progression of lung cancer.

Indexed as

Gene Expression Regulation, NeoplasticAmino Acid SequenceBlotting, WesternCell Line, TumorDNA MethylationDNA Mutational AnalysisDown-RegulationGene ExpressionGene SilencingHumansImmunohistochemistryLung NeoplasmsMembrane ProteinsMolecular Sequence DataNeoplasm ProteinsPromoter Regions, GeneticFXYD3 protein, humanMembrane ProteinsNeoplasm ProteinsRNA, Messenger

Identifiers

PMID19893046
PMCPMC2789644
OpenAlexW67732430

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.