Evidence map›Paper›PMID 28746769›Full record

ArticleCancer science2017

Regulation of spindle and kinetochore-associated protein 1 by antitumor miR-10a-5p in renal cell carcinoma.

Takayuki Arai, Atsushi Okato, Satoko Kojima, Tetsuya Idichi, Keiichi Koshizuka, Akira Kurozumi, Mayuko Kato, Kazuto Yamazaki, Yasuo Ishida, Yukio Naya and 2 more

Open access · goldAbstract read
In one paragraph

Article in Cancer science, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

39 citing papers in PubMed, 60 citations in OpenAlex.

  1. Targeting miRNAs in renal cell carcinoma: emerging therapeutic strategies.International journal of clinical oncology · 2025
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  7. Using the Precision Lasso for gene selection in diffuse large B cell lymphoma cancer.Journal of the Egyptian National Cancer Institute · 2023
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  14. A Review of Recent Research on the Role of MicroRNAs in Renal Cancer.Medical science monitor : international medical journal of experimental and clinical research · 2021
    Review
  15. Article
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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 3 institutions in 1 country.

Takayuki AraiDepartment of Functional Genomics, Chiba University Graduate School of Medicine, Chiba, Japan.ORCID http://orcid.org/0000-0002-3888-9576
Atsushi OkatoDepartment of Functional Genomics, Chiba University Graduate School of Medicine, Chiba, Japan.
Satoko KojimaDepartment of Urology, Teikyo University Chiba Medical Center, Ichihara, Japan.
Tetsuya IdichiDepartment of Digestive Surgery, Breast and Thyroid Surgery, Graduate School of Medical Sciences, Kagoshima University, Kagoshima, Japan.
Keiichi KoshizukaDepartment of Functional Genomics, Chiba University Graduate School of Medicine, Chiba, Japan.ORCID http://orcid.org/0000-0002-0431-8337
Akira KurozumiDepartment of Functional Genomics, Chiba University Graduate School of Medicine, Chiba, Japan.
Mayuko KatoDepartment of Functional Genomics, Chiba University Graduate School of Medicine, Chiba, Japan.
Kazuto YamazakiDepartment of Pathology, Teikyo University Chiba Medical Center, Ichihara, Japan.
Yasuo IshidaDepartment 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.
Chiba University · JPTeikyo University Chiba Medical Center · JPKagoshima University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Analysis of our original microRNA (miRNA) expression signature of patients with advanced renal cell carcinoma (RCC) showed that microRNA-10a-5p (miR-10a-5p) was significantly downregulated in RCC specimens. The aims of the present study were to investigate the antitumor roles of miR-10a-5p and the novel cancer networks regulated by this miRNA in RCC cells. Downregulation of miR-10a-5p was confirmed in RCC tissues and RCC tissues from patients treated with tyrosine kinase inhibitors (TKI). Ectopic expression of miR-10a-5p in RCC cell lines (786-O and A498 cells) inhibited cancer cell migration and invasion. Spindle and kinetochore-associated protein 1 (SKA1) was identified as an antitumor miR-10a-5p target by genome-based approaches, and direct regulation was validated by luciferase reporter assays. Knockdown of SKA1 inhibited cancer cell migration and invasion in RCC cells. Overexpression of SKA1 was observed in RCC tissues and TKI-treated RCC tissues. Moreover, analysis of The Cancer Genome Atlas database demonstrated that low expression of miR-10a-5p and high expression of SKA1 were significantly associated with overall survival in patients with RCC. These findings showed that downregulation of miR-10a-5p and overexpression of the SKA1 axis were highly involved in RCC pathogenesis and resistance to TKI treatment in RCC.

Indexed as

Down-RegulationDrug Resistance, Neoplasm3' Untranslated RegionsAgedAged, 80 and overCarcinoma, Renal CellCell Line, TumorCell MovementChromosomal Proteins, Non-HistoneFemaleGene Expression Regulation, NeoplasticHumansKidney NeoplasmsMaleMicroRNAsMiddle Aged3' Untranslated RegionsChromosomal Proteins, Non-HistoneMicroRNAsMIRN10 microRNA, humanProtein Kinase InhibitorsSKA1 protein, humanMicroRNAmiR-10a-5prenal cell carcinomaspindle and kinetochore-associated protein 1tyrosine kinase inhibitor resistance

Identifiers

PMID28746769
PMCPMC5623743
OpenAlexW2736584458

What OpenQuestion holds

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LicenceCC BY-NC
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.