Evidence map›Paper›PMID 26722360›Full record

ArticleJournal of Cancer2016

The Expression of Ubiquitous Mitochondrial Creatine Kinase Is Downregulated as Prostate Cancer Progression.

Rie Amamoto, Takeshi Uchiumi, Mikako Yagi, Keisuke Monji, YooHyun Song, Yoshinao Oda, Masaki Shiota, Akira Yokomizo, Seiji Naito, Dongchon Kang

Open access · goldAbstract read
In one paragraph

Article in Journal of Cancer, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
0.6field-weighted citation impact, top 32% 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

17 citing papers in PubMed, 30 citations in OpenAlex.

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  7. Role of Serum Creatinine Levels in Prognostic Risk Stratification of Prostate Cancer Patients.Medical science monitor : international medical journal of experimental and clinical research · 2022
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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

10 authors at 2 institutions in 1 country.

Rie Amamoto1. Department of Clinical Chemistry and Laboratory Medicine ; 4. Department of Nutritional Sciences, Seinan Jo Gakuin University, Kitakyushu, Japan.
Takeshi Uchiumi1. Department of Clinical Chemistry and Laboratory Medicine.
Mikako Yagi1. Department of Clinical Chemistry and Laboratory Medicine.
Keisuke Monji1. Department of Clinical Chemistry and Laboratory Medicine.
YooHyun Song2. Department of Anatomic Pathology ; 3. Department of Urology, Kyushu University, Fukuoka, Japan.
Yoshinao Oda2. Department of Anatomic Pathology.
Masaki Shiota3. Department of Urology, Kyushu University, Fukuoka, Japan.
Akira Yokomizo3. Department of Urology, Kyushu University, Fukuoka, Japan.
Seiji Naito3. Department of Urology, Kyushu University, Fukuoka, Japan.
Dongchon Kang1. Department of Clinical Chemistry and Laboratory Medicine.
Kyushu University · JPSeinan Jo Gakuin University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMitochondria play crucial roles in cell signaling events, interorganellar communication, aging, cell proliferation and apoptosis, and mitochondrial impairment has been shown to accelerate or modulate cancer progression. Ubiquitous mitochondrial creatine kinase (uMtCK) is predominantly localized in the intermembrane space of mitochondria and catalyzes the reversible exchange of high-energy phosphate between adenosine tri-phosphate (ATP) and phosphocreatine. However, little is known about its expression and function in human prostate cancer progression.

methodWe investigated the expression of uMtCK in 148 prostate carcinoma tissues and matched normal tissue by immunohistochemistry. The expression and localization of uMtCK and hexokinase II, a marker of glycolysis, were examined in prostate carcinoma cell lines using western blot and immunofluorescence.

resultsMtCK expression was significantly lower in high Gleason grade carcinoma compared with normal prostate or low grade carcinoma. Western blot further revealed that uMtCK was highly expressed in LNCaP and 22Rv1 cell lines, as well as in the normal prostate cell line RWPE-1. However, uMtCK expression was almost absent in PC3 and DU145 cell lines, in correlation with absent or mutant p53 expression, respectively. In contrast, hexokinase II was overexpressed in PC3 cells. Moreover, in the low uMtCK expressing cell lines, glycolytic ATP production was increased, whereas mitochondrial ATP production was decreased.

conclusionsThese data suggest that uMtCK is downregulated as prostate cancer progresses in correlation with a metabolic switch in ATP usage.

Indexed as

ATPmitochondriamtCK

Identifiers

PMID26722360
PMCPMC4679381
OpenAlexW2233416627

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.