Imatinib mesylate promotes melanogenesis through the modulation of p38 and MITF in murine cells.

IF 1.6 4区医学 Q4 TOXICOLOGY Toxicological Research Pub Date : 2024-11-05 eCollection Date: 2025-01-01 DOI:10.1007/s43188-024-00267-8

Natchanok Talapphet, Moon-Moo Kim

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Abstract

Imatinib mesylate is a targeted anti-cancer drug with skin pigmentation as a side effect. The action mechanism of imatinib mesylate on melanogenesis remains unclear. The purpose of this study was to elucidate the mechanism of imatinib mesylate on melanogenesis associated with the microphthalmia-associated transcription factor (MITF) signaling pathway in murine melanoma cells. This study revealed that imatinib mesylate increased tyrosinase activity but decreased hydrogen peroxide generation in B16F1 cells. Additionally, imatinib mesylate at 0.3-5 μM was nontoxic to the cells and promoted melanin production. Moreover, imatinib mesylate at 5 μM increased the expression levels of TRP-2 and p38 related to melanogenesis compared with the blank group in western blot and immunofluorescence staining analyses. The expression level of p-MITF in the nucleus was increased in the presence of imatinib mesylate compared with the blank group. These results suggest that imatinib mesylate could promote melanogenesis through the modulation of p38 and MITF.

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甲磺酸伊马替尼通过调节小鼠细胞中的p38和MITF促进黑色素生成。

甲磺酸伊马替尼是一种靶向抗癌药物，其副作用是皮肤色素沉着。甲磺酸伊马替尼对黑色素形成的作用机制尚不清楚。本研究的目的是阐明甲磺酸伊马替尼对小鼠黑色素瘤细胞中与小眼相关转录因子（MITF）信号通路相关的黑色素生成的作用机制。本研究显示甲磺酸伊马替尼增加了B16F1细胞中酪氨酸酶的活性，但减少了过氧化氢的产生。此外，0.3-5 μM甲磺酸伊马替尼对细胞无毒，并促进黑色素的产生。western blot和免疫荧光染色结果显示，5 μM甲磺酸伊马替尼与空白组相比，增加了与黑色素形成相关的TRP-2和p38的表达水平。与空白组相比，甲磺酸伊马替尼存在时，细胞核中p-MITF的表达水平升高。这些结果表明甲磺酸伊马替尼可能通过调节p38和MITF促进黑色素形成。

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来源期刊

Toxicological Research TOXICOLOGY-

CiteScore

4.20

自引率

4.30%

发文量

期刊介绍： Toxicological Research is the official journal of the Korean Society of Toxicology. The journal covers all areas of Toxicological Research of chemicals, drugs and environmental agents affecting human and animals, which in turn impact public health. The journal’s mission is to disseminate scientific and technical information on diverse areas of toxicological research. Contributions by toxicologists, molecular biologists, geneticists, biochemists, pharmacologists, clinical researchers and epidemiologists with a global view on public health through toxicological research are welcome. Emphasis will be given to articles providing an understanding of the toxicological mechanisms affecting animal, human and public health. In the case of research articles using natural extracts, detailed information with respect to the origin, extraction method, chemical profiles, and characterization of standard compounds to ensure the reproducible pharmacological activity should be provided.