Evidence map›Paper›PMID 23176625›Full record

ArticleCancer science2013

Hedgehog Gli3 activator signal augments tumorigenicity of colorectal cancer via upregulation of adherence-related genes.

Hironori Iwasaki, Kenji Nakano, Kentaro Shinkai, Yumi Kunisawa, Minako Hirahashi, Yoshinao Oda, Hideya Onishi, Mitsuo Katano

Open access · bronzeAbstract read
In one paragraph

Article in Cancer science, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
0.8field-weighted citation impact, top 29% 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, 39 citations in OpenAlex.

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  9. GLI3: a mediator of genetic diseases, development and cancer.Cell communication and signaling : CCS · 2020
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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

8 authors at 2 institutions in 1 country.

Hironori IwasakiDepartment of Cancer Therapy and Research, Kyushu University, Fukuoka, Japan.
Kenji Nakano
Kentaro Shinkai
Yumi Kunisawa
Minako Hirahashi
Yoshinao Oda
Hideya Onishi
Mitsuo Katano
Kyushu University · JPElectronic Navigation Research Institute · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hedgehog signal is re-activated in several cancers. In this study, we examined the role of Gli3 on malignant phenotype of tumorigenicity for colorectal cancer and its relationship with p53, WNT and ERK/AKT signals. Gli3 expression was detected in HT29 and SW480 (p53-mutant) cells, but not in DLD-1 (p53-mutant) or HCT116 (p53-wild type) cells by reverse transcription-polymerase chain reaction and immunocytochemistry. Full-length Gli3 transfection increased anchor-independent growth for all cells regardless of p53 status, with upregulation of adhesion-related genes. Exogenous Sonic-Hedgehog increased activator-type of Gli3 and colony formation in Gli3-positive HT29 and SW480 cells. After implantation of Gli3-FL or mock-transfectant DLD-1 cells into SCID mice, tumor formation was highly observed in only Gli3-FL-transfectant group. In clinical specimens, Gli3 expression was detected in subsets of colorectal cancer and related with poorly-differentiated histological type, while Sonic-Hedgehog was present with high incidence. In conclusion, activator Gli3 signal augments tumorigenicity of colorectal cancer irrespective of p53 status.

Indexed as

AnimalsCell Adhesion MoleculesCell DifferentiationCell Line, TumorColorectal NeoplasmsGene SilencingGenes, p53Hedgehog ProteinsHumansKruppel-Like Transcription FactorsMiceMice, SCIDMutationNeoplasm TransplantationNerve Tissue ProteinsSignal TransductionCell Adhesion MoleculesGLI3 protein, humanHedgehog ProteinsKruppel-Like Transcription FactorsNerve Tissue ProteinsZinc Finger Protein Gli3

Identifiers

PMID23176625
PMCPMC7657255
OpenAlexW1997936966

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.