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G2A as a key modulator of carbonyl stress and apoptosis resistance in glucose-loaded cancer cells
https://tokushima-u.repo.nii.ac.jp/records/2012882
https://tokushima-u.repo.nii.ac.jp/records/201288285dc36b9-9ef1-4896-a40a-c063272ed5c3
| 名前 / ファイル | ライセンス | アクション |
|---|---|---|
bbrc_736_150516.pdf (3 MB)
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| Item type | 文献 / Documents(1) | |||||||||||||||||
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| 公開日 | 2025-04-11 | |||||||||||||||||
| アクセス権 | ||||||||||||||||||
| アクセス権 | open access | |||||||||||||||||
| アクセス権URI | http://purl.org/coar/access_right/c_abf2 | |||||||||||||||||
| 資源タイプ | ||||||||||||||||||
| 資源タイプ識別子 | http://purl.org/coar/resource_type/c_6501 | |||||||||||||||||
| 資源タイプ | journal article | |||||||||||||||||
| 出版社版DOI | ||||||||||||||||||
| 関連識別子 | https://doi.org/10.1016/j.bbrc.2024.150516 | |||||||||||||||||
| 関連名称 | 10.1016/j.bbrc.2024.150516 | |||||||||||||||||
| 出版タイプ | ||||||||||||||||||
| 出版タイプ | VoR | |||||||||||||||||
| 出版タイプResource | http://purl.org/coar/version/c_970fb48d4fbd8a85 | |||||||||||||||||
| タイトル | ||||||||||||||||||
| タイトル | G2A as a key modulator of carbonyl stress and apoptosis resistance in glucose-loaded cancer cells | |||||||||||||||||
| 著者 |
Hassan, Md Abul
× Hassan, Md Abul
× Fukui, Takahito
× Shimizu, Hidetaka
× 岸本, 幸治
WEKO
751
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| 抄録 | ||||||||||||||||||
| 内容記述 | Cancer cells exhibit high glycolytic activity, metabolizing glucose as their primary energy substrate. Toxic metabolites produced during glycolysis, such as methylglyoxal, induce carbonyl stress (CS), promoting inflammation and oxidative stress. The elevated glucose metabolism in cancer cells creates this toxic environment. However, little research has focused on the molecules mediating these reactions and stresses, and their role in selecting and enriching apoptosis-resistant cells. This study investigated the impact of constitutively suppressing oxidized lipid receptor G2A (GPR132) expression on the relationship between CS and oxidative stress in glucose-loaded cancer cells. G2A has recently attracted attention as a tumor promoter. However, our study shows that G2A suppression under glucose loading significantly reduces CS and associated oxidative stress, thereby enhancing cancer cell survival. This suggests a new mechanism contrary to conventional thinking, involving the acute induction of glyoxalase 1 (Glo1). G2A may thus play a role in selecting and enriching apoptosis-resistant cell populations under high glucose conditions by regulating Glo1 expression. These findings improve our understanding of the adaptive capacity of cancer cells to glucose toxicity. | |||||||||||||||||
| キーワード | ||||||||||||||||||
| 主題 | Carbonyl stress | |||||||||||||||||
| キーワード | ||||||||||||||||||
| 主題 | G2A | |||||||||||||||||
| キーワード | ||||||||||||||||||
| 主題 | Glyoxalase 1 | |||||||||||||||||
| キーワード | ||||||||||||||||||
| 主題 | Oxidative stress | |||||||||||||||||
| キーワード | ||||||||||||||||||
| 主題 | Apoptosis resistance | |||||||||||||||||
| 書誌情報 |
en : Biochemical and Biophysical Research Communications 巻 736, p. 150516, 発行日 2024-08-08 |
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| 収録物ID | ||||||||||||||||||
| 収録物識別子タイプ | EISSN | |||||||||||||||||
| 収録物識別子 | 10902104 | |||||||||||||||||
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| 収録物識別子タイプ | PISSN | |||||||||||||||||
| 収録物識別子 | 0006291X | |||||||||||||||||
| 収録物ID | ||||||||||||||||||
| 収録物識別子タイプ | NCID | |||||||||||||||||
| 収録物識別子 | AA11542044 | |||||||||||||||||
| 収録物ID | ||||||||||||||||||
| 収録物識別子タイプ | NCID | |||||||||||||||||
| 収録物識別子 | AA00564395 | |||||||||||||||||
| 出版者 | ||||||||||||||||||
| 出版者 | Elsevier | |||||||||||||||||
| 権利情報 | ||||||||||||||||||
| 権利情報 | This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/). | |||||||||||||||||
| EID | ||||||||||||||||||
| 識別子 | 417161 | |||||||||||||||||
| 言語 | ||||||||||||||||||
| 言語 | eng | |||||||||||||||||
