Evidence map›Paper›PMID 30564899›Full record

ArticleJournal of cancer research and clinical oncology2019

Identification of genes and pathways, including the CXCL2 axis, altered by DNA methylation in hepatocellular carcinoma.

Sophia Subat, Kaoru Mogushi, Mahmut Yasen, Takashi Kohda, Yuichi Ishikawa, Hiroshi Tanaka

Open access · greenAbstract read
In one paragraph

Article in Journal of cancer research and clinical oncology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.8field-weighted citation impact, top 14% 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

19 citing papers in PubMed, 28 citations in OpenAlex.

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  7. Pharmaceuticals (Basel, Switzerland) · 2023
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  18. An Inflammation-Immunity Classifier of 11 Chemokines for Prediction of Overall Survival in Head and Neck Squamous Cell Carcinoma.Medical science monitor : international medical journal of experimental and clinical research · 2019
    Article
  19. 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

6 authors at 2 institutions in 2 countries.

Sophia SubatDepartment of Systems Biology, Graduate School of Biomedical Science, Tokyo Medical and Dental University, Tokyo, Japan.ORCID http://orcid.org/0000-0001-8571-6718
Kaoru MogushiDepartment of Systems Biology, Graduate School of Biomedical Science, Tokyo Medical and Dental University, Tokyo, Japan.
Mahmut YasenDepartment of Systems Biology, Graduate School of Biomedical Science, Tokyo Medical and Dental University, Tokyo, Japan.
Takashi KohdaDepartment of Epigenetics, Graduate School of Biomedical Science, Tokyo Medical and Dental University, Tokyo, Japan.
Yuichi IshikawaDivision of Pathology, The Cancer Institute, Japanese Foundation for Cancer Research, 3-8-31 Ariake, Koto-ward, Tokyo, 135-8550, Japan. ishikawa@jfcr.or.jp.
Hiroshi TanakaDepartment of Systems Biology, Graduate School of Biomedical Science, Tokyo Medical and Dental University, Tokyo, Japan.
Tokyo Medical and Dental University · JPJapanese Foundation For Cancer Research · JP

Funding

Japan Society for the Promotion of Science 15H04714Japan Society for the Promotion of Science JP26870175
6 · The paper itself

Abstract

purposeRecent genetic studies have suggested that tumor suppressor genes are often silenced during carcinogenesis via epigenetic modification caused by methylation of promoter CpG islands. Here, we characterized genes inactivated by DNA methylation in human hepatocellular carcinoma (HCC) to identify the genes and pathways involved in DNA methylation in hepatocellular carcinoma.

methodsEight HCC-derived cell lines were treated with a DNA demethylating agent, 5-aza-2'-deoxycytidine. Additionally, 100 pairs of primary HCC and adjacent non-cancerous tissues as well as 15 normal liver tissues were analyzed by comprehensive gene expression analysis using microarrays. Moreover, gene set enrichment analysis identified the major molecular pathways associated with DNA methylation. Validation of gene expression and DNA methylation status was performed by real-time PCR after bisulfite modification.

resultsWe showed that CXCL2, an immune-related chemokine, expression was significantly downregulated in tumor tissues and also significantly upregulated by DAC treatment in cell lines. Furthermore, we observed a statistically significant difference in methylation status between normal liver tissues and tumor tissues (P < 0.05). In addition, tumors with higher CXCL2 expression included significantly more numbers of multiple tumors than the lower expression group.

conclusionsWe identified CXCL2, an immune-related chemokine, decreased in hepatocellular carcinoma and the regulation mechanism may be controlled by methylation. Further studies should be warranted to examine if and to what extent the gene is actually suppressed by methylation and if there is a possibility that the CXCL2 axis plays a role for diagnosis and treatment of hepatocellular carcinoma.

Indexed as

AdultAgedCarcinoma, HepatocellularChemokine CXCL2CpG IslandsDNA MethylationFemaleGene Expression Regulation, NeoplasticGene SilencingHumansLiver NeoplasmsMaleMiddle AgedChemokine CXCL2CXCL2 protein, humanCXCL2DNA methylationHepatocellular carcinomaInflammationTumor suppressor genes

Identifiers

PMID30564899
PMCPMC11810297
OpenAlexW2904973250

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.