Evidence map›Paper›PMID 26248577›Full record

ArticleMammalian genome : official journal of the International Mammalian Genome Society2015

The oncogenic role of GASC1 in chemically induced mouse skin cancer.

Yumi Ozaki, Kyoko Fujiwara, Maki Ikeda, Toshinori Ozaki, Tadashi Terui, Masayoshi Soma, Johji Inazawa, Hiroki Nagase

Registry-linked trialAbstract read
PubMed Publisher
In one paragraph

Article in Mammalian genome : official journal of the International Mammalian Genome Society, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03070262 (Caffeic Acid for Advanced Esophageal Squamous Cell Cancer), which is not on this map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing 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.

NCT03070262 phase3unknown statusnot on this mapstarted 2017, after this paper: background citation

Caffeic Acid for Advanced Esophageal Squamous Cell Cancer: A Randomized, Double-blind, and Multicenter Trial in Chinese Patients

TypeinterventionalSponsorThe First Affiliated Hospital of Henan University of Science and TechnologyRan2017 to 2021Enrolled300ConditionsEsophagus CancerArmsCA, placebo group
3 · Its place in the literature

Who cites it

5 citing papers in PubMed, 12 citations in OpenAlex.

  1. Kdm4d mutant mice show impaired sperm motility and subfertility.The Journal of reproduction and development · 2024
    Article
  2. Article
  3. KDM4 Demethylases: Structure, Function, and Inhibitors.Advances in experimental medicine and biology · 2023
    Article
  4. Article
  5. Review
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 3 institutions in 1 country.

Yumi OzakiDepartment of Dermatology, Nihon University Graduate School of Medicine, Tokyo, Japan.
Kyoko FujiwaraDivision of General Medicine, Department of Medicine, Nihon University School of Medicine, 30-1 Oyaguchi-Kamicho, Itabashi, Tokyo, 173-8610, Japan. fujiwara.kyoko@nihon-u.ac.jp.
Maki IkedaDivision of Public Health, Department of Social Medicine, Nihon University School of Medicine, Tokyo, Japan.
Toshinori OzakiLaboratory of DNA Damage Signaling, Chiba Cancer Center Research Institute, Chiba, Japan.
Tadashi TeruiDepartment of Dermatology, Nihon University Graduate School of Medicine, Tokyo, Japan.
Masayoshi SomaDivision of General Medicine, Department of Medicine, Nihon University School of Medicine, 30-1 Oyaguchi-Kamicho, Itabashi, Tokyo, 173-8610, Japan.
Johji InazawaDepartment of Molecular Cytogenetics, Medical Research Institute, Tokyo Medical and Dental University, Tokyo, Japan.
Hiroki NagaseLaboratory of Cancer Genetics, Chiba Cancer Center Research Institute, Chiba, Japan. hnagase@chiba-cc.jp.
Nihon University · JPChiba Cancer Center · JPTokyo Medical and Dental University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Gene amplified in squamous cell carcinoma (SCC) 1 (GASC1), also known as KDM4C/JMJD2C, encodes a histone demethylase that specifically demethylates lysine residues (H3K9, H3K36, and H1.4K26) and plays a crucial role in the regulation of gene expression as well as in heterochromatin formation. GASC1 is located at human chromosome 9p23-24, where frequent genomic amplification is observed in human esophageal cancer, and its aberrant expression is detected in a variety of human cancers, such as breast, colon, and prostate. Therefore, it is highly likely that GASC1 contributes to the genesis and/or development of cancer. However, there is a lack of direct evidence of GASC1 having an oncogenic function. In this study, we aimed to clarify the role of GASC1 in the skin SCC carcinogenesis. For this purpose, we generated Gasc1-heterozygous mice (Gasc1+/-) with reduced expression of Gasc1. On the basis of our results, Gasc1+/- mice displayed a significantly lower incidence and multiplicity of both benign and malignant tumors induced by the two-stage skin carcinogenesis protocol than wild-type mice. In addition, the volume of carcinoma was significantly lower in Gasc1+/- mice. Consistent with these observations, knocking down of Gasc1 resulted in reduced cell viability of SCC cells in vitro. Our findings clearly demonstrated that GASC1 has an oncogenic role in skin carcinogenesis.

Indexed as

9,10-Dimethyl-1,2-benzanthraceneAnimalsCarcinogenesisCell Line, TumorCell SurvivalFemaleGenetic Association StudiesGenetic Predisposition to DiseaseJumonji Domain-Containing Histone DemethylasesMaleMice, Inbred C57BLMice, KnockoutOncogenesPapillomaSkin NeoplasmsTumor Burden9,10-Dimethyl-1,2-benzanthraceneJmjd2c protein, mouseJumonji Domain-Containing Histone Demethylases

Identifiers

PMID26248577
OpenAlexW1088813759

What OpenQuestion holds

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Registered trials

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.