alfa-Tokoferylsukcinát inhibuje angiogenezu přerušením parakrinních FGF2- signálních drah

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F68378050%3A_____%2F07%3A00096529" target="_blank" >RIV/68378050:_____/07:00096529 - isvavai.cz</a>

Výsledek na webu

—

DOI - Digital Object Identifier

—

Jazyk výsledku

angličtina

Název v původním jazyce

alpha-Tocopheryl succinate inhibits angiogenesis by disrupting paracrine FGF2 signalling

Popis výsledku v původním jazyce

The so-called mitocans from the vitamin E group of selective anticancer drugs, ?-tocopheryl succinate (?-TOS) and its ether analogue ?-TEA, triggered apoptosis in proliferating but not arrested endothelial cells. Angiogenic endothelial cells exposed to the vitamin E analogues, unlike their arrested counterparts, readily accumulated ROS by interfering with the mitochondrial redox chain and activating the intrinsic apoptotic pathway. The vitamin E analogues inhibited angiogenesis in vitro as assessed using the ?wound-healing? and ?tube-forming? models. Endothelial cells deficient in mitochondrial DNA were resistant to the vitamin E analogues, both in ROS accumulation and apoptosis induction, maintaining their high angiogenic potential. ?-TOS inhibited angiogenesis in a mouse cancer model, as documented by ultrasound imaging. We conclude that vitamin E analogues selectively kill angiogenic endothelial cells, suppressing tumor growth, which has intriguing clinical implications.

Název v anglickém jazyce

alpha-Tocopheryl succinate inhibits angiogenesis by disrupting paracrine FGF2 signalling

Popis výsledku anglicky

The so-called mitocans from the vitamin E group of selective anticancer drugs, ?-tocopheryl succinate (?-TOS) and its ether analogue ?-TEA, triggered apoptosis in proliferating but not arrested endothelial cells. Angiogenic endothelial cells exposed to the vitamin E analogues, unlike their arrested counterparts, readily accumulated ROS by interfering with the mitochondrial redox chain and activating the intrinsic apoptotic pathway. The vitamin E analogues inhibited angiogenesis in vitro as assessed using the ?wound-healing? and ?tube-forming? models. Endothelial cells deficient in mitochondrial DNA were resistant to the vitamin E analogues, both in ROS accumulation and apoptosis induction, maintaining their high angiogenic potential. ?-TOS inhibited angiogenesis in a mouse cancer model, as documented by ultrasound imaging. We conclude that vitamin E analogues selectively kill angiogenic endothelial cells, suppressing tumor growth, which has intriguing clinical implications.

Druh

J_x - Nezařazeno - Článek v odborném periodiku (Jimp, Jsc a Jost)

CEP obor

EB - Genetika a molekulární biologie

OECD FORD obor

—

Projekt

—

Návaznosti

Z - Vyzkumny zamer (s odkazem do CEZ)

Rok uplatnění

2007

Kód důvěrnosti údajů

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

Název periodika

FEBS Letters

ISSN

0014-5793

e-ISSN

—

Svazek periodika

581

Číslo periodika v rámci svazku

24

Stát vydavatele periodika

GB - Spojené království Velké Británie a Severního Irska

Počet stran výsledku

5

Strana od-do

4611-4615

Kód UT WoS článku

—

EID výsledku v databázi Scopus

—