Evidence map›Paper›PMID 16767159›Full record

ArticleOncogene2006

Suppression of tumorigenicity, but not anchorage independence, of human cancer cells by new candidate tumor suppressor gene CapG.

A Watari, K Takaki, S Higashiyama, Y Li, Y Satomi, T Takao, A Tanemura, Y Yamaguchi, I Katayama, M Shimakage and 4 more

Abstract read
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In one paragraph

Article in Oncogene, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.8field-weighted citation impact, top 16% 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, 38 citations in OpenAlex.

  1. Article
  2. FYB1-targeted modulation of CAPG promotes AML progression.Molecular and cellular biochemistry · 2025
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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

14 authors at 4 institutions in 1 country.

A WatariResearch Institute for Microbial Diseases, Osaka University, Suita, Osaka, Japan.
K Takaki
S Higashiyama
Y Li
Y Satomi
T Takao
A Tanemura
Y Yamaguchi
I Katayama
M Shimakage
I Miyashiro
K Takami
K Kodama
M Yutsudo
Osaka University · JPOsaka Medical Center for Cancer and Cardiovascular Diseases · JPOsaka National Hospital · JPProtein Research Foundation · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Previously, we isolated a series of cell lines from a human diploid fibroblast lineage as a model for multistep tumorigenesis in humans. After passaging a single LT-transfected fibroblast clone, differently progressed cell lines were obtained, including immortalized, anchorage-independent and tumorigenic cell lines. In the present paper, we analysed the gene expression profiles of these model cell lines, and observed that expression of the CapG protein was lost in the tumorigenic cell line. To examine the possibility that loss of CapG protein expression was required for tumorigenic progression, we transfected CapG cDNA into the tumorigenic cell line and tested for tumor-forming ability in nude mice. Results showed that ectopic expression of CapG suppressed tumorigenicity, but not growth in soft agar or liquid medium. We also found that certain cancer cell lines including stomach cancer, lung cancer and melanoma had also lost CapG expression. One such cancer cell line AZ521 also became non-tumorigenic after the introduction of CapG cDNA. Moreover, we showed that CapG expression was repressed in small-cell lung cancer tissues. Together, our findings indicated that CapG is a new tumor suppressor gene involved in the tumorigenic progression of certain cancers.

Indexed as

Cell Transformation, NeoplasticGenes, Tumor SuppressorAnimalsBlotting, SouthernBlotting, WesternCell AdhesionCell Line, TumorCell MovementCulture MediaHumansMiceMice, NudeMicrofilament ProteinsNeoplasmsNuclear ProteinsCAPG protein, humanCulture MediaMicrofilament ProteinsNuclear Proteins

Identifiers

PMID16767159
OpenAlexW1965235911

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.