MAZ靶向上调NDUFS3表达促进黑色素瘤恶性进展的分子机制。

IF 5.2 1区 生物学 Q1 BIOLOGY
Yu Feng, Qinxuan Ni, Na Wu, Taiyu Xie, Fang Yun, Xuedan Zhang, Lingnan Gao, Yanlong Gai, Enjiang Li, Xiaojia Yi, Junlin Xie, Qiao Zhang, Zhe Yang, Buqing Sai, Yingmin Kuang, Yuechun Zhu
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引用次数: 0

摘要

Myc相关锌指蛋白(MAZ)与多种肿瘤的恶性进展有关。然而,MAZ在黑色素瘤中的表达及其功能关系此前尚未得到研究。本研究证实,MAZ在黑色素瘤中的高表达与患者的不良预后相关。此外,我们的研究结果表明,MAZ 可通过促进增殖、迁移和侵袭来加强黑色素瘤的进展。值得注意的是,我们发现MAZ可以靶向调节线粒体复合物I的核心亚基NADH脱氢酶[泛醌]铁硫蛋白3(NDUFS3)的转录,从而增强线粒体代谢,进而促进黑色素瘤的恶性进展。预测模型表明,MAZ和NDUFS3的共同表达可作为黑色素瘤患者的潜在预后标志物。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Molecular mechanisms of MAZ targeting up-regulation of NDUFS3 expression to promote malignant progression in melanoma.

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.

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来源期刊
Communications Biology
Communications Biology Medicine-Medicine (miscellaneous)
CiteScore
8.60
自引率
1.70%
发文量
1233
审稿时长
13 weeks
期刊介绍: Communications Biology is an open access journal from Nature Research publishing high-quality research, reviews and commentary in all areas of the biological sciences. Research papers published by the journal represent significant advances bringing new biological insight to a specialized area of research.
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