Evidence map›Paper›PMID 29196733›Full record

ArticleJournal of human genetics2018

Regulation of HMGB3 by antitumor miR-205-5p inhibits cancer cell aggressiveness and is involved in prostate cancer pathogenesis.

Yasutaka Yamada, Rika Nishikawa, Mayuko Kato, Atsushi Okato, Takayuki Arai, Satoko Kojima, Kazuto Yamazaki, Yukio Naya, Tomohiko Ichikawa, Naohiko Seki

Abstract read
PubMed Publisher
In one paragraph

Article in Journal of human genetics, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

51 citing papers in PubMed, 66 citations in OpenAlex.

  1. Article
  2. Review
  3. Overview of high mobility group box 3 (HMGB3] protein.Molecular genetics and genomics : MGG · 2025
    Review
  4. Structure and Functions of HMGB3 Protein.International journal of molecular sciences · 2024
    Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Review
  12. The expression of high mobility group protein 3 (American journal of cancer research · 2023
    Article
  13. Article
  14. microRNA-205 in prostate cancer: Overview to clinical translation.Biochimica et biophysica acta. Reviews on cancer · 2022
    Review
  15. Article
  16. Review
  17. Review
  18. Article
  19. Article
  20. 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.

Yasutaka YamadaDepartment of Functional Genomics, Chiba University Graduate School of Medicine, Chiba, Japan.ORCID http://orcid.org/0000-0002-0070-1590
Rika NishikawaDepartment of Functional Genomics, Chiba University Graduate School of Medicine, Chiba, Japan.
Mayuko KatoDepartment of Functional Genomics, Chiba University Graduate School of Medicine, Chiba, Japan.
Atsushi OkatoDepartment of Functional Genomics, Chiba University Graduate School of Medicine, Chiba, Japan.
Takayuki AraiDepartment of Functional Genomics, Chiba University Graduate School of Medicine, Chiba, Japan.
Satoko KojimaDepartment of Urology, Teikyo University Chiba Medical Center, Ichihara, Japan.
Kazuto YamazakiDepartment of Pathology, Teikyo University Chiba Medical Center, Ichihara, Japan.
Yukio NayaDepartment of Urology, Teikyo University Chiba Medical Center, Ichihara, Japan.
Tomohiko IchikawaDepartment of Urology, Chiba University Graduate School of Medicine, Chiba, Japan.
Naohiko SekiDepartment of Functional Genomics, Chiba University Graduate School of Medicine, Chiba, Japan. naoseki@faculty.chiba-u.jp.
Chiba University · JPTeikyo University Chiba Medical Center · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Our recent determination of a microRNA (miRNA) expression signature in prostate cancer (PCa) revealed that miR-205-5p was significantly reduced in PCa tissues and that it acted as an antitumor miRNA. The aim of this study was to identify oncogenic genes and pathways in PCa cells that were regulated by antitumor miR-205-5p. Genome-wide gene expression analyses and in silico miRNA database searches showed that 37 genes were putative targets of miR-205-5p regulation. Among those genes, elevated expression levels of seven in particular (HMGB3, SPARC, MKI67, CENPF, CDK1, RHOU, and POLR2D) were associated with a shorter disease-free survival in a large number of patients in the The Cancer Genome Atlas (TCGA) database. We focused on high-mobility group box 3 (HMGB3) because it was the most downregulated by ectopic expression of miR-205-5p in PC3 cells and its expression was involved in PCa pathogenesis. Luciferase reporter assays showed that HMGB3 was directly regulated by miR-205-5p in PCa cells. Knockdown studies using si-HMGB3 showed that expression of HMGB3 enhanced PCa cell aggressiveness. Overexpression of HMGB3/HMGB3 was confirmed in naive PCa and castration-resistant PCa (CRPC) clinical specimens. Novel approaches to analysis of antitumor miRNA-regulated RNA networks in PCa cells may provide new insights into the pathogenic mechanisms of the disease.

Indexed as

Genes, Tumor SuppressorProstatic Neoplasms, Castration-ResistantCell Line, TumorHMGB3 ProteinHumansMaleMicroRNAsNeoplasm ProteinsRNA, NeoplasmHMGB3 ProteinMicroRNAsMIR205, humanNeoplasm ProteinsRNA, Neoplasm

Identifiers

PMID29196733
OpenAlexW2771276814

What OpenQuestion holds

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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.