Evidence map›Paper›PMID 40013327›Full record

ArticleCancer medicine2025

DGKα Enhances Tumorigenic Activity in Bladder Cancer Patients With Chronic Kidney Disease.

Kenshiro Takemoto, Kohei Kobatake, Tomoya Hatayama, Shinsaku Tasaka, Mai Okazaki, Yoshinori Nakano, Hiroyuki Shikuma, Kazuma Yukihiro, Kyosuke Iwane, Ryoken Yamanaka and 10 more

Abstract read
In one paragraph

Article in Cancer medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
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

20 authors.

Kenshiro TakemotoDepartment of Urology, Graduate School of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.ORCID https://orcid.org/0000-0002-9077-4733
Kohei KobatakeDepartment of Urology, Graduate School of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.
Tomoya HatayamaDepartment of Urology, Graduate School of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.
Shinsaku TasakaDepartment of Urology, Graduate School of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.
Mai OkazakiDepartment of Urology, Graduate School of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.
Yoshinori NakanoDepartment of Urology, Graduate School of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.
Hiroyuki ShikumaDepartment of Urology, Graduate School of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.
Kazuma YukihiroDepartment of Urology, Graduate School of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.
Kyosuke IwaneDepartment of Urology, Graduate School of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.
Ryoken YamanakaDepartment of Urology, Graduate School of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.
Ryo TasakaDepartment of Urology, Graduate School of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.
Yuki KohadaDepartment of Urology, Graduate School of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.
Miki NaitoDepartment of Urology, Graduate School of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.
Shunsuke MiyamotoDepartment of Urology, Graduate School of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.
Yohei SekinoDepartment of Urology, Graduate School of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.
Hiroyuki KitanoDepartment of Urology, Graduate School of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.ORCID https://orcid.org/0000-0003-2223-2403
Keisuke GotoDepartment of Urology, Graduate School of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.
Akihiro GorikiDepartment of Urology, Graduate School of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.
Keisuke HiedaDepartment of Urology, Graduate School of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.
Nobuyuki HinataDepartment of Urology, Graduate School of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.ORCID https://orcid.org/0000-0001-7014-6812

Funding

Japan Society for the Promotion of Science 21K15506
6 · The paper itself

Abstract

introductionChronic kidney disease (CKD) is a risk factor for bladder cancer (BC) and is reportedly involved in its recurrence and progression. This study aimed to determine the molecular mechanisms underlying the development of BC in patients with CKD.

methodsFirst, we generated the CKD mouse model according to a unilateral two-stage renal ischemia-reperfusion injury protocol using wild-type C57BL/6 mice. Second, we conducted a molecular functional analysis of DGKα in BC and investigated the contribution of DGKα to cell invasion, migration, and proliferation activity using human BC cell lines.

resultsAfter confirming elevated serum creatinine levels in mice, the bladder was dissected, and mRNA sequencing of bladder urothelial cells was conducted. Gene expression profiling revealed remarkable upregulation in diacylglycerol kinase alpha (DGKα) level compared to that in control urothelial cells. DGKα-knockdown cells displayed significantly decreased invasion, migration, and proliferation activity compared to the controls. Next, we conducted a clinical analysis of DGKα in BC patients and performed immunohistochemistry (IHC) on samples from patients treated with radical cystectomy. IHC staining revealed that DGKα-positive cases had significantly worse recurrence-free and cancer-specific survival rates (p = 0.036 and = 0.003, respectively).

conclusionDGKα expression is associated with tumorigenic activity in BC. Therefore, it is speculated that increased expression of DGKα in CKD cases is involved in the malignant potentials in BC. In conclusion, the crucial role of DGKα in BC is suggested, and it may be one of the factors contributing to poor prognosis in BC patients with CKD.

Indexed as

Diacylglycerol KinaseRenal Insufficiency, ChronicUrinary Bladder NeoplasmsAgedAnimalsCell Line, TumorCell MovementCell ProliferationDisease Models, AnimalFemaleHumansMaleMiceMice, Inbred C57BLMiddle AgedDiacylglycerol Kinasebladder cancerchronic kidney diseasetumorigenic activity

Identifiers

PMID40013327
PMCPMC11865707

What Socratic holds

Textmetadata
LicenceCC BY
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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 Socratic graph.