Functional mitochondrial respiration is essential for glioblastoma tumour growth
Identifikátory výsledku
Kód výsledku v IS VaVaI
<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F68378041%3A_____%2F25%3A00637936" target="_blank" >RIV/68378041:_____/25:00637936 - isvavai.cz</a>
Nalezeny alternativní kódy
RIV/86652036:_____/25:00637936 RIV/68378050:_____/25:00637936 RIV/00216208:11110/25:10497830 RIV/00216208:11130/25:10497830 a 2 dalších
Výsledek na webu
<a href="https://www.nature.com/articles/s41388-025-03429-6" target="_blank" >https://www.nature.com/articles/s41388-025-03429-6</a>
DOI - Digital Object Identifier
<a href="http://dx.doi.org/10.1038/s41388-025-03429-6" target="_blank" >10.1038/s41388-025-03429-6</a>
Alternativní jazyky
Jazyk výsledku
angličtina
Název v původním jazyce
Functional mitochondrial respiration is essential for glioblastoma tumour growth
Popis výsledku v původním jazyce
Horizontal transfer of mitochondria from the tumour microenvironment to cancer cells to support proliferation and enhance tumour progression has been shown for various types of cancer in recent years. Glioblastoma, the most aggressive adult brain tumour, has proven to be no exception when it comes to dynamic intercellular mitochondrial movement, as shown in this study using an orthotopic tumour model of respiration-deficient glioblastoma cells. Although confirmed mitochondrial transfer was shown to facilitate tumour progression in glioblastoma, we decided to investigate whether the related electron transport chain recovery is necessary for tumour formation in the brain. Based on experiments using time-resolved analysis of tumour formation by glioblastoma cells depleted of their mitochondrial DNA, we conclude that functional mitochondrial respiration is essential for glioblastoma growth in vivo, because it is needed to support coenzyme Q redox cycling for de novo pyrimidine biosynthesis controlled by respiration-linked dihydroorotate dehydrogenase enzyme activity. We also demonstrate here that astrocytes are key mitochondrial donors in this model.
Název v anglickém jazyce
Functional mitochondrial respiration is essential for glioblastoma tumour growth
Popis výsledku anglicky
Horizontal transfer of mitochondria from the tumour microenvironment to cancer cells to support proliferation and enhance tumour progression has been shown for various types of cancer in recent years. Glioblastoma, the most aggressive adult brain tumour, has proven to be no exception when it comes to dynamic intercellular mitochondrial movement, as shown in this study using an orthotopic tumour model of respiration-deficient glioblastoma cells. Although confirmed mitochondrial transfer was shown to facilitate tumour progression in glioblastoma, we decided to investigate whether the related electron transport chain recovery is necessary for tumour formation in the brain. Based on experiments using time-resolved analysis of tumour formation by glioblastoma cells depleted of their mitochondrial DNA, we conclude that functional mitochondrial respiration is essential for glioblastoma growth in vivo, because it is needed to support coenzyme Q redox cycling for de novo pyrimidine biosynthesis controlled by respiration-linked dihydroorotate dehydrogenase enzyme activity. We also demonstrate here that astrocytes are key mitochondrial donors in this model.
Klasifikace
Druh
J<sub>imp</sub> - Článek v periodiku v databázi Web of Science
CEP obor
—
OECD FORD obor
10608 - Biochemistry and molecular biology
Návaznosti výsledku
Projekt
Výsledek vznikl pri realizaci vícero projektů. Více informací v záložce Projekty.
Návaznosti
I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace
Ostatní
Rok uplatnění
2025
Kód důvěrnosti údajů
S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů
Údaje specifické pro druh výsledku
Název periodika
Oncogene
ISSN
0950-9232
e-ISSN
1476-5594
Svazek periodika
44
Číslo periodika v rámci svazku
30
Stát vydavatele periodika
DE - Spolková republika Německo
Počet stran výsledku
16
Strana od-do
2588-2603
Kód UT WoS článku
001481335300001
EID výsledku v databázi Scopus
2-s2.0-105004356661