Evidence map›Paper›PMID 41436878›Full record

ArticleAnalytical and bioanalytical chemistry2025

LC-MS/MS and high-spatial single-cell MSI reveal selective downregulation of PC(16:0_16:0) and PC(18:0_18:1) due to mPGES-1 knockdown in hormone-resistant prostate cancer cell line.

Mst Sayela Afroz, Shuhei Aramaki, Md Muedur Rahman, Maxime Dubail, Zhang Chi, Kyoka Fujii, Mariko Kurosawa, Keita Tamura, Tomoaki Kahyo, Katsumasa Nakamura and 4 more

Abstract read
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In one paragraph

Article in Analytical and bioanalytical chemistry, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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.

Mst Sayela AfrozDepartment of Cellular and Molecular Anatomy, Hamamatsu University School of Medicine, 1-20-1 Handayama, Chuo-Ku, Hamamatsu, Shizuoka, 431-3125, Japan.
Shuhei AramakiPhotonic Quantum Therapeutics Laboratory, Institute of Photonics Medicine, Hamamatsu University School of Medicine, 1-20-1 Handayama, Chuo-Ku, Hamamatsu, Shizuoka, 431-3125, Japan. aramaki@hama-med.ac.jp.ORCID http://orcid.org/0000-0001-5842-6176
Md Muedur RahmanDepartment of Cellular and Molecular Anatomy, Hamamatsu University School of Medicine, 1-20-1 Handayama, Chuo-Ku, Hamamatsu, Shizuoka, 431-3125, Japan.
Maxime DubailDepartment of Cellular and Molecular Anatomy, Hamamatsu University School of Medicine, 1-20-1 Handayama, Chuo-Ku, Hamamatsu, Shizuoka, 431-3125, Japan.
Zhang ChiDepartment of Cellular and Molecular Anatomy, Hamamatsu University School of Medicine, 1-20-1 Handayama, Chuo-Ku, Hamamatsu, Shizuoka, 431-3125, Japan.
Kyoka FujiiGraduate School of Life Science, Showa Women's University, 1-7-57 Taishido, Setagaya-Ku, Tokyo, Japan.
Mariko KurosawaGraduate School of Life Science, Showa Women's University, 1-7-57 Taishido, Setagaya-Ku, Tokyo, Japan.
Keita TamuraDepartment of Urology, Hamamatsu University School of Medicine, 1-20-1 Handayama, Chuo-Ku, Hamamatsu, Shizuoka, 431-3125, Japan.
Tomoaki KahyoDepartment of Cellular and Molecular Anatomy, Hamamatsu University School of Medicine, 1-20-1 Handayama, Chuo-Ku, Hamamatsu, Shizuoka, 431-3125, Japan.
Katsumasa NakamuraDepartment of Radiation Oncology, Hamamatsu University School of Medicine, 1-20-1 Handayama, Chuo-Ku, Hamamatsu, Shizuoka, 431-3125, Japan.
Teruo InamotoDepartment of Urology, Hamamatsu University School of Medicine, 1-20-1 Handayama, Chuo-Ku, Hamamatsu, Shizuoka, 431-3125, Japan.
Olof RådmarkDivision of Physiological Chemistry II, Department of Medical Biochemistry and Biophysics, Karolinska Institute, 171 77, Stockholm, Sweden.
Mitsutoshi SetouDepartment of Cellular and Molecular Anatomy, Hamamatsu University School of Medicine, 1-20-1 Handayama, Chuo-Ku, Hamamatsu, Shizuoka, 431-3125, Japan.
Hiromi HanakaGraduate School of Life Science, Showa Women's University, 1-7-57 Taishido, Setagaya-Ku, Tokyo, Japan. h-hanaka@swu.ac.jp.

Funding

Japan Agency for Medical Research and Development 21ak0101179Japan Society for the Promotion of Science JP22H02793Japan Society for the Promotion of Science JP23K18197Japan Society for the Promotion of Science J-PEAKSProgram on Open Innovation Platform with Enterprises, Research Institute and Academia JPMXS0450200225
6 · The paper itself

Abstract

Prostate cancer is one of the most common cancers in men, and 10-20% of cases progress to a hormone-resistant form, posing a major therapeutic challenge. The microsomal prostaglandin E2 synthase-1 (mPGES-1), a key enzyme in prostaglandin E2 biosynthesis from arachidonic acid, has been predicted as a therapeutic target in suppressing prostate cancer. However, the impact of mPGES-1 on the cellular lipidome has not been systematically investigated. Here, this study applied LC-MS/MS analysis and high-spatial single-cell mass spectrometry imaging (MSI) analysis using atmospheric pressure matrix-assisted laser desorption/ionization-MSI (AP-MALDI-MSI) to investigate the role of the mPGES-1 gene in altering the lipidome of hormone-resistant DU145 prostate cancer cells. LC-MS/MS results revealed significant downregulation of phosphatidylcholine (PC) and triglyceride (TG) species, and upregulation of ceramide species in KD (stable knockdown of the mPGES-1 gene) compared to controls. Upregulation of PCs is the signature of the tumor microenvironment of prostate cancer cells, and the upregulated ceramides are associated with programmed cell death. Consistent findings were observed in high-spatial single-cell MSI analysis for PC(16:0_16:0) and PC(18:0_18:1), which were significantly (p < 0.001) downregulated in KD compared to controls, and also revealed a striking loss of metabolic heterogeneity of these PC molecules. The loss of metabolic heterogeneity due to mPGES-1 knockdown may reduce cancer cells' adaptive capacity, suggesting mPGES-1 inhibition as a strategy to overcome metabolic plasticity in hormone-resistant prostate cancer. Thus, this study highlights that suppressing mPGES-1 can be a future therapeutic target in preventing the progression of hormone-resistant prostate cancer development.

Indexed as

AP-MALDI-MSILipidomicsmPGES-1PhosphatidylcholineProstate cancerSingle-cell MSI

Identifiers

PMID41436878

What Socratic holds

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Registered trials

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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 Socratic graph.