Chelidonine and Homochelidonine Induce Cell Death through Cell Cycle Checkpoints and MAP Kinase Pathways

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00216275%3A25310%2F17%3A39910661" target="_blank" >RIV/00216275:25310/17:39910661 - isvavai.cz</a>

Nalezeny alternativní kódy

RIV/00216208:11150/17:10363744 RIV/00216208:11160/17:10363744

Výsledek na webu

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DOI - Digital Object Identifier

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Jazyk výsledku

angličtina

Název v původním jazyce

Chelidonine and Homochelidonine Induce Cell Death through Cell Cycle Checkpoints and MAP Kinase Pathways

Popis výsledku v původním jazyce

This study focuses on the comparative in vitro cytotoxicity of chelidonine and homochelidonine on human cancer and non-cancer cells. Both alkaloids produced a decrease in cellular growth in a dose-dependent manner exhibiting greater potency in cancer cells. The growth inhibitory effect was evidenced in both ovarian carcinoma A2780 and lung fibroblast MRC-5 cells by inducing G2 and mitotic phase cell cycle arrest. Results indicated that the extent of apoptosis induced by chelidonine and homochelidonine was correlated to sensitivity to the antiproliferative activity of the evaluated compounds. Western blotting suggested that the cellular toxicological mechanism of chelidonine is related to the differential upregulation of phospho-Chk2, p21(Cip1/Waf1), phospho-ERK1/2 and phospho-p38 in various cell types, leading to alternations in the suppression of proliferation and either induction or prevention of apoptosis. Chelidonine showed the more potent effects and also affected the cell cycle checkpoints and MAPK signaling pathways within cells.

Název v anglickém jazyce

Chelidonine and Homochelidonine Induce Cell Death through Cell Cycle Checkpoints and MAP Kinase Pathways

Popis výsledku anglicky

This study focuses on the comparative in vitro cytotoxicity of chelidonine and homochelidonine on human cancer and non-cancer cells. Both alkaloids produced a decrease in cellular growth in a dose-dependent manner exhibiting greater potency in cancer cells. The growth inhibitory effect was evidenced in both ovarian carcinoma A2780 and lung fibroblast MRC-5 cells by inducing G2 and mitotic phase cell cycle arrest. Results indicated that the extent of apoptosis induced by chelidonine and homochelidonine was correlated to sensitivity to the antiproliferative activity of the evaluated compounds. Western blotting suggested that the cellular toxicological mechanism of chelidonine is related to the differential upregulation of phospho-Chk2, p21(Cip1/Waf1), phospho-ERK1/2 and phospho-p38 in various cell types, leading to alternations in the suppression of proliferation and either induction or prevention of apoptosis. Chelidonine showed the more potent effects and also affected the cell cycle checkpoints and MAPK signaling pathways within cells.

Druh

J_imp - Článek v periodiku v databázi Web of Science

CEP obor

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OECD FORD obor

30107 - Medicinal chemistry

Projekt

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Návaznosti

I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Rok uplatnění

2017

Kód důvěrnosti údajů

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

Název periodika

Natural Product Communications

ISSN

1934-578X

e-ISSN

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Svazek periodika

12

Číslo periodika v rámci svazku

9

Stát vydavatele periodika

US - Spojené státy americké

Počet stran výsledku

12

Strana od-do

1419-1430

Kód UT WoS článku

000412968400010

EID výsledku v databázi Scopus

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