Evidence map›Paper›PMID 20454511›Full record

ArticleNeoplasia (New York, N.Y.)2010

Three-dimensionally specific inhibition of DNA repair-related genes by activated KRAS in colon crypt model.

Toshiyuki Tsunoda, Yasuo Takashima, Takahiro Fujimoto, Midori Koyanagi, Yasuhiro Yoshida, Keiko Doi, Yoko Tanaka, Masahide Kuroki, Takehiko Sasazuki, Senji Shirasawa

Open access · goldAbstract read
In one paragraph

Article in Neoplasia (New York, N.Y.), 2010. 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
2.1field-weighted citation impact, top 13% 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, 48 citations in OpenAlex.

  1. Article
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  3. Effects ofMicroorganisms · 2021
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  4. Predicting the Role of DNA Polymerase β Alone or withJournal of clinical medicine · 2020
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  16. The interconnectedness of cancer cell signaling.Neoplasia (New York, N.Y.) · 2011
    Article
  17. Article
  18. Article
  19. Article
  20. Immune-related zinc finger gene ZFAT is an essential transcriptional regulator for hematopoietic differentiation in blood islands.Proceedings of the National Academy of Sciences of the United States of America · 2010
    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

10 authors at 2 institutions in 1 country.

Toshiyuki TsunodaDepartment of Cell Biology, Faculty of Medicine, Fukuoka University, Fukuoka, Japan.
Yasuo Takashima
Takahiro Fujimoto
Midori Koyanagi
Yasuhiro Yoshida
Keiko Doi
Yoko Tanaka
Masahide Kuroki
Takehiko Sasazuki
Senji Shirasawa
Fukuoka University · JPSaitama International Medical Center · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Growth and differentiation of colonic epithelium are regulated in the three-dimensional (3D) physiological architecture, colonic crypt, and deregulation of 3D interactions is involved in tumorigenesis. Cell-based 3D culture systems provide a suitable approach bridging the gap between two-dimensional (2D) culture and animal models. KRAS mutations are found at high frequencies in human colorectal cancer (CRC); however, KRAS-targeted cancer therapy has not been developed. Here, we have established a 3D cell culture model resembling the colonic crypt by use of HKe3 cells, human CRC HCT116 cells disrupted at activated KRAS. In this 3D colonic crypt model, HKe3 cells showed the features of time course-dependent transit-amplifying and terminal-differentiated stages, which are characteristic of normal colonic crypt. On the basis of the features of HCT116 cells, activated KRAS inhibited normal cell polarity and apoptosis in 3D culture. The expression of DNA repair-related tumor suppressor genes including TP53, BRCA1, BRCA2, and EXO-1 was markedly suppressed by activated KRAS in 3D culture but not in 2D culture. These results together suggest that activated KRAS plays critical roles in the accumulation of genetic alterations through inhibition of DNA repair genes and apoptosis and that this 3D culture model will provide a useful tool for investigating the molecular mechanisms of CRC development.

Indexed as

ApoptosisBlotting, WesternCell Culture TechniquesCell Line, TumorColorectal NeoplasmsDNA RepairDNA Repair EnzymesFluorescent Antibody TechniqueGene ExpressionGene Expression ProfilingHumansIntestinal MucosaMicroscopy, ConfocalModels, BiologicalProto-Oncogene ProteinsProto-Oncogene Proteins p21(ras)DNA Repair EnzymesKRAS protein, humanProto-Oncogene ProteinsProto-Oncogene Proteins p21(ras)ras Proteins

Identifiers

PMID20454511
PMCPMC2864477
OpenAlexW1957830733

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.