Horizontal transfer of whole mitochondria restores tumorigenic potential in mitochondria! DNA-deficient cancer cells

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F86652036%3A_____%2F17%3A00474268" target="_blank" >RIV/86652036:_____/17:00474268 - isvavai.cz</a>

Nalezeny alternativní kódy

RIV/68378050:_____/17:00474268 RIV/00216208:11310/17:10359229

Výsledek na webu

<a href="http://dx.doi.org/10.7554/eLife.22187" target="_blank" >http://dx.doi.org/10.7554/eLife.22187</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.7554/eLife.22187" target="_blank" >10.7554/eLife.22187</a>

Jazyk výsledku

angličtina

Název v původním jazyce

Horizontal transfer of whole mitochondria restores tumorigenic potential in mitochondria! DNA-deficient cancer cells

Popis výsledku v původním jazyce

Recently, we showed that generation of tumours in syngeneic mice by cells devoid of mitochondrial (mt) DNA (rho(0) cells) is linked to the acquisition of the host mtDNA. However, the mechanism of mtDNA movement between cells remains unresolved. To determine whether the transfer of mtDNA involves whole mitochondria, we injected B16 rho(0) mouse melanoma cells into syngeneic C576116N(su9DsRed2) mice that express red fluorescent protein in their mitochondria. We document that mtDNA is acquired by transfer of whole mitochondria from the host animal, leading to normalisation of mitochondrial respiration. Additionally, knockdown of key mitochondrial complex I (NDUFV1) and complex II (SDHC) subunits by shRNA in B16 rho(0) cells abolished or significantly retarded their ability to form tumours. Collectively, these results show that intact mitochondria with their mtDNA payload are transferred in the developing tumour, and provide functional evidence for an essential role of oxidative phosphorylation in cancer.

Název v anglickém jazyce

Horizontal transfer of whole mitochondria restores tumorigenic potential in mitochondria! DNA-deficient cancer cells

Popis výsledku anglicky

Recently, we showed that generation of tumours in syngeneic mice by cells devoid of mitochondrial (mt) DNA (rho(0) cells) is linked to the acquisition of the host mtDNA. However, the mechanism of mtDNA movement between cells remains unresolved. To determine whether the transfer of mtDNA involves whole mitochondria, we injected B16 rho(0) mouse melanoma cells into syngeneic C576116N(su9DsRed2) mice that express red fluorescent protein in their mitochondria. We document that mtDNA is acquired by transfer of whole mitochondria from the host animal, leading to normalisation of mitochondrial respiration. Additionally, knockdown of key mitochondrial complex I (NDUFV1) and complex II (SDHC) subunits by shRNA in B16 rho(0) cells abolished or significantly retarded their ability to form tumours. Collectively, these results show that intact mitochondria with their mtDNA payload are transferred in the developing tumour, and provide functional evidence for an essential role of oxidative phosphorylation in cancer.

Druh

J_imp - Článek v periodiku v databázi Web of Science

CEP obor

—

OECD FORD obor

10608 - Biochemistry and molecular biology

Projekt

Výsledek vznikl pri realizaci vícero projektů. Více informací v záložce Projekty.

Návaznosti

P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)

Rok uplatnění

2017

Kód důvěrnosti údajů

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Název periodika

eLife

ISSN

2050-084X

e-ISSN

—

Svazek periodika

6

Číslo periodika v rámci svazku

15 Febr 2017

Stát vydavatele periodika

US - Spojené státy americké

Počet stran výsledku

22

Strana od-do

—

Kód UT WoS článku

000397644600001

EID výsledku v databázi Scopus

2-s2.0-85016312406