Evidence map›Paper›PMID 30228364›Full record

ArticleJournal of human genetics2018

Molecular pathogenesis of triple-negative breast cancer based on microRNA expression signatures: antitumor miR-204-5p targets AP1S3.

Hiroko Toda, Sasagu Kurozumi, Yuko Kijima, Tetsuya Idichi, Yoshiaki Shinden, Yasutaka Yamada, Takayuki Arai, Kosei Maemura, Takaaki Fujii, Jun Horiguchi and 2 more

Abstract read
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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 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

36 citing papers in PubMed, 52 citations in OpenAlex.

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  11. LINC00562 drives gastric cancer development by regulating miR-4636-AP1S3 axis.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2023
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  20. Impact of Oncogenic Targets by Tumor-SuppressiveInternational journal of molecular sciences · 2021
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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

12 authors at 4 institutions in 1 country.

Hiroko TodaDepartment of Digestive Surgery, Breast and Thyroid Surgery, Graduate School of Medical and Dental Sciences, Kagoshima University, Kagoshima, Japan.
Sasagu KurozumiDepartment of General Surgical Science, Gunma University Graduate School of Medicine, Gunma, Japan.
Yuko KijimaDepartment of Digestive Surgery, Breast and Thyroid Surgery, Graduate School of Medical and Dental Sciences, Kagoshima University, Kagoshima, Japan.
Tetsuya IdichiDepartment of Digestive Surgery, Breast and Thyroid Surgery, Graduate School of Medical and Dental Sciences, Kagoshima University, Kagoshima, Japan.
Yoshiaki ShindenDepartment of Digestive Surgery, Breast and Thyroid Surgery, Graduate School of Medical and Dental Sciences, Kagoshima University, Kagoshima, Japan.
Yasutaka YamadaDepartment of Functional Genomics, Chiba University Graduate School of Medicine, Chiba, Japan.
Takayuki AraiDepartment of Functional Genomics, Chiba University Graduate School of Medicine, Chiba, Japan.
Kosei MaemuraDepartment of Digestive Surgery, Breast and Thyroid Surgery, Graduate School of Medical and Dental Sciences, Kagoshima University, Kagoshima, Japan.
Takaaki FujiiDepartment of General Surgical Science, Gunma University Graduate School of Medicine, Gunma, Japan.
Jun HoriguchiDepartment of Breast Surgery, International University of Health and Welfare, Chiba, Japan.
Shoji NatsugoeDepartment of Digestive Surgery, Breast and Thyroid Surgery, Graduate School of Medical and Dental Sciences, Kagoshima University, Kagoshima, Japan.
Naohiko SekiDepartment of Functional Genomics, Chiba University Graduate School of Medicine, Chiba, Japan. naoseki@faculty.chiba-u.jp.
Kagoshima University · JPChiba University · JPGunma University · JPInternational University of Health and Welfare · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Triple-negative breast cancer (TNBC) is an aggressive type of cancer associated with a poor prognosis. Identification of novel therapeutic targets in TNBC is urgently needed. Here, we investigated the microRNA (miRNA) expression signature of TNBC using clinical specimens. In total, 104 miRNAs (56 upregulated and 48 downregulated) were significantly dysregulated in TNBC tissues; miR-204-5p showed the most dramatic downregulation. We then examined the antitumor roles of miR-204-5p in breast cancer (BC) cells. Notably, cancer cell migration and invasion were significantly reduced by ectopic expression of miR-204-5p in BC cells. Genome-wide gene expression analysis and in silico database search revealed that 32 genes were putative miR-204-5p targets. High expression of AP1S3, RACGAP1, ELOVL6, and LRRC59 was significantly associated with poor prognosis in patients with BC, and adaptor-related protein complex 1 sigma 3 subunit (AP1S3) was directly regulated by miR-204-5p, as demonstrated by luciferase reporter assays. AP1S3 overexpression was detected in TNBC clinical specimens and enhanced cancer cell aggressiveness. We further analyzed downstream RNA networks regulated by AP1S3 in BC cells. Overall, this miRNA signature is expected to be an effective tool for identification of miRNA-mediated molecular mechanisms of TNBC pathogenesis.

Indexed as

Cell MovementGene Expression Regulation, NeoplasticCell Line, TumorFemaleGenome-Wide Association StudyHumansMicroRNAsNeoplasm InvasivenessNeoplasm ProteinsRNA, NeoplasmTriple Negative Breast NeoplasmsMicroRNAsMIRN204 microRNA, humanNeoplasm ProteinsRNA, Neoplasm

Identifiers

PMID30228364
OpenAlexW2892181499

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.