Evidence map›Paper›PMID 30701354›Full record

ArticleJournal of neuro-oncology2019

MicroRNA regulating stanniocalcin-1 is a metastasis and dissemination promoting factor in glioblastoma.

Junichi Sakata, Takashi Sasayama, Kazuhiro Tanaka, Hiroaki Nagashima, Mitsutoshi Nakada, Hirotomo Tanaka, Naoya Hashimoto, Naoki Kagawa, Manabu Kinoshita, Satoshi Nakamizo and 4 more

Abstract read
PubMed Publisher
In one paragraph

Article in Journal of neuro-oncology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
0.7field-weighted citation impact, top 37% 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

18 citing papers in PubMed, 21 citations in OpenAlex.

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  15. miR-137: A Novel Therapeutic Target for Human Glioma.Molecular therapy. Nucleic acids · 2020
    Review
  16. Review
  17. Expression, function and clinical application of stanniocalcin-1 in cancer.Journal of cellular and molecular medicine · 2020
    Review
  18. 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

14 authors at 5 institutions in 1 country.

Junichi SakataDepartment of Neurosurgery, Kobe University Graduate School of Medicine, 7-5-1, Kusunoki-cho, Chuo-ku, Kobe, 650-0017, Japan.
Takashi SasayamaDepartment of Neurosurgery, Kobe University Graduate School of Medicine, 7-5-1, Kusunoki-cho, Chuo-ku, Kobe, 650-0017, Japan. takasasa@med.kobe-u.ac.jp.ORCID http://orcid.org/0000-0002-5593-9045
Kazuhiro TanakaDepartment of Neurosurgery, Kobe University Graduate School of Medicine, 7-5-1, Kusunoki-cho, Chuo-ku, Kobe, 650-0017, Japan.
Hiroaki NagashimaDepartment of Neurosurgery, Kobe University Graduate School of Medicine, 7-5-1, Kusunoki-cho, Chuo-ku, Kobe, 650-0017, Japan.
Mitsutoshi NakadaDepartment of Neurosurgery, Kanazawa University, Kanazawa, Japan.
Hirotomo TanakaDepartment of Neurosurgery, Kobe University Graduate School of Medicine, 7-5-1, Kusunoki-cho, Chuo-ku, Kobe, 650-0017, Japan.
Naoya HashimotoDepartment of Neurosurgery, Kyoto Prefectural University Graduate School of Medical Science, Kyoto, Japan.
Naoki KagawaDepartment of Neurosurgery, Osaka University Graduate School of Medicine, Suita, Japan.
Manabu KinoshitaDepartment of Neurosurgery, Osaka University Graduate School of Medicine, Suita, Japan.
Satoshi NakamizoDepartment of Neurosurgery, Kobe University Graduate School of Medicine, 7-5-1, Kusunoki-cho, Chuo-ku, Kobe, 650-0017, Japan.
Masahiro MaeyamaDepartment of Neurosurgery, Kobe University Graduate School of Medicine, 7-5-1, Kusunoki-cho, Chuo-ku, Kobe, 650-0017, Japan.
Masamitsu NishiharaDepartment of Neurosurgery, West Kobe Medical Center, Kobe, Japan.
Kohkichi HosodaDepartment of Neurosurgery, West Kobe Medical Center, Kobe, Japan.
Eiji KohmuraDepartment of Neurosurgery, Kobe University Graduate School of Medicine, 7-5-1, Kusunoki-cho, Chuo-ku, Kobe, 650-0017, Japan.
Kobe University · JPKobe Medical Center · JPThe University of Osaka · JPKanazawa University · JPKyoto Prefectural University · JP

Funding

the Japanese Ministry of Education, Culture, Sports, Science, and Technology 15K10332the Japanese Ministry of Education, Culture, Sports, Science, and Technology 16K20010the Japanese Ministry of Education, Culture, Sports, Science, and Technology 17K10863the Japanese Ministry of Education, Culture, Sports, Science, and Technology 17K10864the Japanese Ministry of Education, Culture, Sports, Science, and Technology 17K10898the Japanese Ministry of Education, Culture, Sports, Science, and Technology 17K16648
6 · The paper itself

Abstract

backgroundMicroRNAs (miRs) regulate many biological processes, such as invasion, angiogenesis, and metastasis. Glioblastoma (GBM) patients with metastasis/metastatic dissemination have a very poor prognosis; therefore, inhibiting metastasis/metastatic dissemination has become an important therapeutic strategy for GBM treatment.

methodsUsing 76 GBM tissues, we examined the expression levels of 23 GBM-related miRs and compared the miRs' expression levels between GBMs with metastasis/metastatic dissemination and GBMs without metastasis/metastatic dissemination. Using the bioinformatics web site, we searched the target genes of miRs. To analyze the function of target gene, several biological assays and survival analysis by the Kaplan-Meier method were performed.

resultsWe found that eight miRs were significantly decreased in GBM with metastasis/metastatic dissemination. By the bioinformatics analysis, we identified stanniocalcin-1 (STC1) as the most probable target gene against the combination of these miRs. Four miRs (miR-29B, miR-34a, miR-101, and miR-137) have predictive binding sites in STC1 mRNA, and mRNA expression of STC1 was downregulated by mimics of these miRs. Also, mimics of these miRs and knockdown of STC1 by siRNA suppressed invasion in GBM cells. GBM with metastasis/metastatic dissemination had significantly higher levels of STC1 than GBM without metastasis/metastatic dissemination. Finally, Kaplan-Meier analysis demonstrated that GBMs with high STC1 level had significantly shorter survival than GBMs with low STC1 level.

conclusionsSTC1 may be a novel metastasis/metastatic dissemination promoting factor regulated by several miRs in GBM. Because STC1 is a secreted glycoprotein and functions via the autocrine/paracrine signals, inhibiting STC1 signal may become a novel therapeutic strategy for GBM.

Indexed as

AdolescentAdultAgedAged, 80 and overBrain NeoplasmsCell Line, TumorCell MovementCohort StudiesComputational BiologyFemaleGene Expression Regulation, NeoplasticGlioblastomaGlycoproteinsHumansMaleMicroRNAsGlycoproteinsMicroRNAsteleocalcinBiomarkerDisseminationGlioblastomaMetastasesMicroRNASTC1

Identifiers

PMID30701354
OpenAlexW2912196891

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.