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MAZ 靶向调控 NDUFS3 表达促进黑色素瘤恶性进展的分子机制。

Molecular mechanisms of MAZ targeting up-regulation of NDUFS3 expression to promote malignant progression in melanoma.

机构信息

Department of Biochemistry and Molecular Biology, School of Basic Medicine, Kunming Medical University, Kunming, China.

Department of Pathology, The Second Affiliated Hospital of Kunming Medical University, Kunming, China.

出版信息

Commun Biol. 2024 Nov 12;7(1):1491. doi: 10.1038/s42003-024-07209-y.

Abstract

Myc-associated Zinc-finger Protein (MAZ) has been implicated in the malignant progression of various tumors. However, its expression and functional relationship of MAZ in melanoma have not been previously investigated. This study confirms elevated expression of MAZ in melanoma, correlating with poor patient prognosis. Furthermore, our findings demonstrate that MAZ enhances melanoma progression by promoting proliferation, migration and invasion. It is worth noting that we found that MAZ can target and regulate the transcription of NADH dehydrogenase [ubiquinone] iron-sulfur protein 3 (NDUFS3), a core subunit of mitochondrial complex I, to enhance mitochondrial metabolism and thus promote malignant progression of melanoma. Predictive modeling indicates that the co-expression of MAZ and NDUFS3 could serve as a potential prognostic marker for melanoma patients.

摘要

Myc 相关锌指蛋白(MAZ)已被牵涉到多种肿瘤的恶性进展中。然而,MAZ 在黑色素瘤中的表达和功能关系尚未被研究。本研究证实 MAZ 在黑色素瘤中高表达,与患者预后不良相关。此外,我们的研究结果表明 MAZ 通过促进增殖、迁移和侵袭来增强黑色素瘤的进展。值得注意的是,我们发现 MAZ 可以靶向并调节 NADH 脱氢酶[泛醌]铁硫蛋白 3(NDUFS3)的转录,NDUFS3 是线粒体复合物 I 的核心亚基,以增强线粒体代谢,从而促进黑色素瘤的恶性进展。预测模型表明 MAZ 和 NDUFS3 的共表达可能成为黑色素瘤患者的潜在预后标志物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9bda/11557950/cd2bce258b55/42003_2024_7209_Fig1_HTML.jpg

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