The adaptor protein Miro1 modulates horizontal transfer of mitochondria in mouse melanoma models.

IF 6.9 1区生物学 Q1 CELL BIOLOGY Cell reports Pub Date : 2025-01-28 Epub Date: 2025-01-09 DOI:10.1016/j.celrep.2024.115154

Jaromir Novak, Zuzana Nahacka, Gabriela L Oliveira, Petra Brisudova, Maria Dubisova, Sarka Dvorakova, Sona Miklovicova, Marketa Dalecka, Verena Puttrich, Lenka Grycova, Silvia Magalhaes-Novais, Catarina Mendes Correia, Jennifer Levoux, Ludek Stepanek, Jan Prochazka, David Svec, David Pajuelo Reguera, Guillermo Lopez-Domenech, Renata Zobalova, Radek Sedlacek, Mikkel G Terp, Payam A Gammage, Zdenek Lansky, Josef Kittler, Paulo J Oliveira, Henrik J Ditzel, Michael V Berridge, Anne-Marie Rodriguez, Stepana Boukalova, Jakub Rohlena, Jiri Neuzil

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Abstract

Recent research has shown that mtDNA-deficient cancer cells (ρ⁰ cells) acquire mitochondria from tumor stromal cells to restore respiration, facilitating tumor formation. We investigated the role of Miro1, an adaptor protein involved in movement of mitochondria along microtubules, in this phenomenon. Inducible Miro1 knockout (Miro1^KO) mice markedly delayed tumor formation after grafting ρ⁰ cancer cells. Miro1^KO mice with fluorescently labeled mitochondria revealed that this delay was due to hindered mitochondrial transfer from the tumor stromal cells to grafted B16 ρ⁰ cells, which impeded recovery of mitochondrial respiration and tumor growth. Miro1^KO led to the perinuclear accumulation of mitochondria and impaired mobility of the mitochondrial network. In vitro experiments revealed decreased association of mitochondria with microtubules, compromising mitochondrial transfer via tunneling nanotubes (TNTs) in mesenchymal stromal cells. Here we show the role of Miro1 in horizontal mitochondrial transfer in mouse melanoma models in vivo and its involvement with TNTs.

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在小鼠黑色素瘤模型中，接头蛋白Miro1调节线粒体的水平转移。

最近的研究表明，mtdna缺失的癌细胞（ρ0细胞）从肿瘤基质细胞获得线粒体，恢复呼吸，促进肿瘤的形成。我们研究了Miro1的作用，一种参与线粒体沿微管运动的衔接蛋白，在这种现象中。诱导型Miro1敲除（Miro1KO）小鼠移植ρ0癌细胞后肿瘤形成明显延迟。线粒体荧光标记的Miro1KO小鼠发现，这种延迟是由于线粒体从肿瘤基质细胞转移到移植的B16 ρ0细胞受阻，从而阻碍了线粒体呼吸和肿瘤生长的恢复。Miro1KO导致核周线粒体积聚和线粒体网络的移动性受损。体外实验显示，线粒体与微管的关联减弱，损害了间充质基质细胞中通过隧道纳米管（TNTs）进行的线粒体转移。在这里，我们展示了Miro1在小鼠黑色素瘤模型体内水平线粒体转移中的作用及其与tnt的参与。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Cell reports CELL BIOLOGY-

CiteScore

13.80

自引率

1.10%

发文量

1305

审稿时长

77 days

期刊介绍： Cell Reports publishes high-quality research across the life sciences and focuses on new biological insight as its primary criterion for publication. The journal offers three primary article types: Reports, which are shorter single-point articles, research articles, which are longer and provide deeper mechanistic insights, and resources, which highlight significant technical advances or major informational datasets that contribute to biological advances. Reviews covering recent literature in emerging and active fields are also accepted. The Cell Reports Portfolio includes gold open-access journals that cover life, medical, and physical sciences, and its mission is to make cutting-edge research and methodologies available to a wide readership. The journal's professional in-house editors work closely with authors, reviewers, and the scientific advisory board, which consists of current and future leaders in their respective fields. The advisory board guides the scope, content, and quality of the journal, but editorial decisions are independently made by the in-house scientific editors of Cell Reports.