Evidence map›Paper›PMID 16479256›Full record

ArticleBritish journal of cancer2006

Ubiquitous mitochondrial creatine kinase downregulated in oral squamous cell carcinoma.

T Onda, K Uzawa, Y Endo, H Bukawa, H Yokoe, T Shibahara, H Tanzawa

Open access · hybridAbstract read
In one paragraph

Article in British journal of cancer, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 1 pooled it
2.3field-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

26 citing papers in PubMed, 1 synthesis or guideline pooled it, 71 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Ubiquitous mitochondrial creatine kinase promotes the progression of gastric cancer through a JNK-MAPK/JUN/HK2 axis regulated glycolysis.Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 2023
    Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Observational
  15. Article
  16. Article
  17. Article
  18. ALY as a potential contributor to metastasis in human oral squamous cell carcinoma.Journal of cancer research and clinical oncology · 2013
    Article
  19. Article
  20. Tripeptidyl peptidase II in human oral squamous cell carcinoma.Journal of cancer research and clinical oncology · 2013
    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 3 institutions in 1 country.

T OndaDepartment of Oral and Maxillo-Facial Surgery, Tokyo Dental College, 1-2-2 Masago, Mihama-ku Chiba 261-8502, Japan.
K Uzawa
Y Endo
H Bukawa
H Yokoe
T Shibahara
H Tanzawa
Chiba University Hospital · JPChiba University · JPTokyo Dental College · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In this study, we performed two-dimensional electrophoresis (2-DE) and matrix-assisted laser desorption/ionisation time of fly mass spectrometry to identify the protein(s) associated with the development of oral squamous cell carcinomas (OSCCs) by comparing patterns of OSCC-derived cell lines with normal oral keratinocytes (NOKs), and found that downregulation of ubiquitous mitochondrial creatine kinase (CKMT1) could be a good candidate. Decreased levels of CKMT1 mRNA and protein were detected in all OSCC-derived cell lines examined (n=9) when compared to those in primary normal oral keratinocytes. Although no sequence variation in the coding region of the CKMT1 gene with the exception of a nonsense mutation in exon 8 was identified in these cell lines, we found a frequent hypermethylation in the CpG island region. CKMT1 expression was restored by experimental demethylation. In addition, when we transfected CKMT1 into the cell lines, they showed an apoptotic phenotype but no invasiveness. In clinical samples, high frequencies of CKMT1 downregulation were detected by immunohistochemistry (19 of 52 (37%)) and quantitative real-time RT-PCR (21 of 50 (42%)). Furthermore, the CKMT1 expression status was significantly correlated with tumour differentiation (P<0.0001). These results suggest that the CKMT1 gene is frequently inactivated during oral carcinogenesis and that an epigenetic mechanism may regulate loss of expression, which may lead to block apoptosis.

Indexed as

Gene Expression Regulation, NeoplasticApoptosisCarcinoma, Squamous CellCell Line, TumorCpG IslandsCreatine Kinase, Mitochondrial FormDNA MethylationDown-RegulationElectrophoresis, Gel, Two-DimensionalExonsGene Expression ProfilingHumansImmunohistochemistryKeratinocytesMouth NeoplasmsReverse Transcriptase Polymerase Chain ReactionCreatine Kinase, Mitochondrial FormRNA, Messenger

Identifiers

PMID16479256
PMCPMC2361206
OpenAlexW2047382816

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.