Evidence map›Paper›PMID 28418868›Full record

ArticleOncotarget2017

GRIK2 has a role in the maintenance of urothelial carcinoma stem-like cells, and its expression is associated with poorer prognosis.

Ryuta Inoue, Yoshihiko Hirohashi, Hiroshi Kitamura, Sachiyo Nishida, Aiko Murai, Akari Takaya, Eri Yamamoto, Masahiro Matsuki, Toshiaki Tanaka, Terufumi Kubo and 6 more

Abstract read
In one paragraph

Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
–field-weighted citation impact
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

10 citing papers in PubMed.

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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

16 authors.

Ryuta InoueDepartment of Pathology, Sapporo Medical University School of Medicine, Chuo-Ku, Sapporo 060-8556, Japan.
Yoshihiko HirohashiDepartment of Pathology, Sapporo Medical University School of Medicine, Chuo-Ku, Sapporo 060-8556, Japan.
Hiroshi KitamuraDepartment of Urology, Graduate School of Medicine and Pharmaceutical Science for Research, University of Toyama, Toyama-Shi 930-0194, Japan.
Sachiyo NishidaDepartment of Pathology, Sapporo Medical University School of Medicine, Chuo-Ku, Sapporo 060-8556, Japan.
Aiko MuraiDepartment of Pathology, Sapporo Medical University School of Medicine, Chuo-Ku, Sapporo 060-8556, Japan.
Akari TakayaDepartment of Pathology, Sapporo Medical University School of Medicine, Chuo-Ku, Sapporo 060-8556, Japan.
Eri YamamotoDepartment of Pathology, Sapporo Medical University School of Medicine, Chuo-Ku, Sapporo 060-8556, Japan.
Masahiro MatsukiDepartment of Pathology, Sapporo Medical University School of Medicine, Chuo-Ku, Sapporo 060-8556, Japan.
Toshiaki TanakaDepartment of Urology, Sapporo Medical University School of Medicine, Chuo-Ku, Sapporo 060-8556, Japan.
Terufumi KuboDepartment of Pathology, Sapporo Medical University School of Medicine, Chuo-Ku, Sapporo 060-8556, Japan.
Munehide NakatsugawaDepartment of Pathology, Sapporo Medical University School of Medicine, Chuo-Ku, Sapporo 060-8556, Japan.
Takayuki KanasekiDepartment of Pathology, Sapporo Medical University School of Medicine, Chuo-Ku, Sapporo 060-8556, Japan.
Tomohide TsukaharaDepartment of Pathology, Sapporo Medical University School of Medicine, Chuo-Ku, Sapporo 060-8556, Japan.
Noriyuki SatoDepartment of Pathology, Sapporo Medical University School of Medicine, Chuo-Ku, Sapporo 060-8556, Japan.
Naoya MasumoriDepartment of Urology, Sapporo Medical University School of Medicine, Chuo-Ku, Sapporo 060-8556, Japan.
Toshihiko TorigoeDepartment of Pathology, Sapporo Medical University School of Medicine, Chuo-Ku, Sapporo 060-8556, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cancer stem-like cells (CSCs)/cancer-initiating cells (CICs) are small sub-population of cancer cells that are endowed with higher tumor-initiating ability, self-renewal ability and differentiation ability. CSCs/CICs could be isolated as high aldehyde dehydrogenase 1 activity cells (ALDH1high) from various cancer samples. In this study, we isolated urothelial carcinoma CSCs/CICs as ALDHhigh cells and investigated the molecular aspects. ALDH1high cells showed greater sphere-forming ability and higher tumor-initiating ability in immune-deficient mice than those of ALDH1low cells, indicating that CSCs/CICs were enriched in ALDH1high cells. cDNA microarray analysis revealed that an ionotropic glutamate receptor glutamate receptor, ionotropic, kainate 2 (GRIK2) was expressed in ALDH1high cells at a higher level than that in ALDH1low cells. GRIK2 gene knockdown by siRNAs decreased the sphere-forming ability and invasion ability, whereas GRIK2 overexpression increased the sphere-forming ability, invasion ability and tumorigenicity, indicating that GRIK2 has a role in the maintenance of CSCs/CICs. Immunohistochemical staining revealed that higher levels of GRIK2 and ALDH1 expression were related to poorer prognosis in urinary tract carcinoma cases. The findings indicate that GRIK2 has a role in the maintenance of urothelial CSCs/CICs and that GRIK2 and ALDH1 can be prognosis prediction markers for urinary tract carcinomas.

Indexed as

Aldehyde Dehydrogenase 1 FamilyAnimalsCarcinogenesisCell Line, TumorCell Self RenewalFemaleGene Expression Regulation, NeoplasticGluK2 Kainate ReceptorHumansIsoenzymesKainic Acid ReceptorsMiceMice, SCIDNeoplastic Stem CellsPrognosisRetinal DehydrogenaseAldehyde Dehydrogenase 1 FamilyALDH1A1 protein, humanALDH1A1 protein, mouseGluK2 Kainate ReceptorIsoenzymesKainic Acid ReceptorsRetinal DehydrogenaseRNA, Small InterferingALDH1cancer stem-like cellsGRIK2urothelial carcinoma

Identifiers

PMID28418868
PMCPMC5438695

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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.