Evidence map›Paper›PMID 41632438›Full record

ArticleCell biochemistry and biophysics2026

Characterization of Novel Decenoic Acid Derivatives Exhibiting Cytotoxic Activity Against T98G Glioma Cells Under a Serum- and Glucose-deprived Condition.

Yuma Ito, Norihiro Tada, Chihiro Muraki, Yuta Kubota, Mahmoud Kandeel, Yukio Kitade, Akichika Itoh, Kentaro Oh-Hashi

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Article in Cell biochemistry and biophysics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
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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

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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

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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

8 authors.

Yuma ItoGraduate School of Natural Science and Technology, Gifu University, 1-1 Yanagido, Gifu, 501-1193, Japan.
Norihiro TadaLaboratory of Pharmaceutical Synthetic Chemistry, Faculty of Pharmaceutical Science, Gifu Pharmaceutical University, 1-25-4 Daigaku-nishi, Gifu, 501-1196, Japan.
Chihiro MurakiLaboratory of Pharmaceutical Synthetic Chemistry, Faculty of Pharmaceutical Science, Gifu Pharmaceutical University, 1-25-4 Daigaku-nishi, Gifu, 501-1196, Japan.
Yuta KubotaLaboratory of Pharmaceutical Synthetic Chemistry, Faculty of Pharmaceutical Science, Gifu Pharmaceutical University, 1-25-4 Daigaku-nishi, Gifu, 501-1196, Japan.
Mahmoud KandeelDepartment of Biomedical Sciences, College of Veterinary Medicine, King Faisal University, Al-Ahsa, 31982, Saudi Arabia.
Yukio KitadeDepartment of Materials Chemistry, Graduate School of Engineering, Aichi Institute of Technology, 1247 Yachigusa, Yakusacho, 470-0392, Toyota, Japan.
Akichika ItohLaboratory of Pharmaceutical Synthetic Chemistry, Faculty of Pharmaceutical Science, Gifu Pharmaceutical University, 1-25-4 Daigaku-nishi, Gifu, 501-1196, Japan.
Kentaro Oh-HashiGraduate School of Natural Science and Technology, Gifu University, 1-1 Yanagido, Gifu, 501-1193, Japan. oh-hashi.kentaro.u7@f.gifu-u.ac.jp.

Funding

Grants-in-aid from the Japan Society for the Promotion of Science KAKENHI, no. 25K03045the Deanship of Scientific Research, Vice Presidency for Graduate Studies and Scientific Research, King Faisal University Grant No. KFU253294
6 · The paper itself

Abstract

The proliferative capacity and drug resistance of cancer cells are thought to be related to adaptations to the low nutrient and hypoxic conditions known as the tumor microenvironment. This adaptation is suggested to involve the unfolded protein response (UPR) triggered by the endoplasmic reticulum (ER) stress. Therefore, the ER stress induced under these conditions is considered one of the attractive targets for antitumor drug development. In this study, we designed and synthesized decenoic acid derivatives and found two compounds, 13-Chloro-6-(4-fluorophenoxy)tridec-6-en-8-yn-1-ol (Cpd6) and 13-Chloro-6-(4-methoxyphenoxy)tridec-6-en-8-yn-1-ol (Cpd2) showed cytotoxicity against human glioma cell-line, T98G, under the serum- and glucose-deprived condition. These two compounds exerted inhibitory effects on several ER and Golgi stress responses triggered under this low-nutrient condition. Furthermore, Cpd6 profoundly downregulated the expression of c-Myc protein, a well-known oncogenic factor, in T98G cells. This study is expected to contribute to the development of fatty acid-derived antitumor compounds targeting the ER and Golgi stress responses.

Indexed as

Antineoplastic AgentsFatty Acids, MonounsaturatedGliomaGlucoseCell Line, TumorCell SurvivalEndoplasmic Reticulum StressHumansProto-Oncogene Proteins c-mycUnfolded Protein ResponseAntineoplastic AgentsFatty Acids, MonounsaturatedGlucoseProto-Oncogene Proteins c-mycDecenoic acid derivativeGliomaStress responseTumor microenvironmentsUPR

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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.