Targeting cancer cells through antibiotics-induced mitochondrial dysfunction requires autophagy inhibition

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00216224%3A14110%2F17%3A00096272" target="_blank" >RIV/00216224:14110/17:00096272 - isvavai.cz</a>

Výsledek na webu

<a href="http://dx.doi.org/10.1016/j.canlet.2016.09.023" target="_blank" >http://dx.doi.org/10.1016/j.canlet.2016.09.023</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1016/j.canlet.2016.09.023" target="_blank" >10.1016/j.canlet.2016.09.023</a>

Jazyk výsledku

angličtina

Název v původním jazyce

Targeting cancer cells through antibiotics-induced mitochondrial dysfunction requires autophagy inhibition

Popis výsledku v původním jazyce

A significant part of current research studies utilizes various cellular models which imply specific antibiotics-containing media as well as antibiotics used for clonal selection or promoter de/activation. With the great success of developing such tools, mitochondria, once originated from bacteria, can be effectively targeted by antibiotics. For that reason, some studies propose antibiotics-targeting of mitochondria as part of anticancer therapy. Here, we have focused on the effects of various classes of antibiotics on mitochondria in cancer and non-cancer cells and demonlow mitochondrial membrane potential, reduced ATP production, altered morphology and lowered respiration rate which altogether suggested mitochondrial dysfunction (MDF). This was in parallel with increased level of reactive oxygen species (ROS) and decreased activity of mitochondria( respiration complexes. However, both survival and repopulation capacity of cancer cells was not significantly affected by the antibiotics, perhaps due to a glycolytic shift or activated autophagy. In turn, simultaneous inhibition of autophagy and treatment with antibiotics largely reduced tumorigenic properties of cancer cells suggesting potential strategy for anticancer therapy. (C) 2016 Published by Elsevier Ireland Ltd.

Název v anglickém jazyce

Targeting cancer cells through antibiotics-induced mitochondrial dysfunction requires autophagy inhibition

Popis výsledku anglicky

A significant part of current research studies utilizes various cellular models which imply specific antibiotics-containing media as well as antibiotics used for clonal selection or promoter de/activation. With the great success of developing such tools, mitochondria, once originated from bacteria, can be effectively targeted by antibiotics. For that reason, some studies propose antibiotics-targeting of mitochondria as part of anticancer therapy. Here, we have focused on the effects of various classes of antibiotics on mitochondria in cancer and non-cancer cells and demonlow mitochondrial membrane potential, reduced ATP production, altered morphology and lowered respiration rate which altogether suggested mitochondrial dysfunction (MDF). This was in parallel with increased level of reactive oxygen species (ROS) and decreased activity of mitochondria( respiration complexes. However, both survival and repopulation capacity of cancer cells was not significantly affected by the antibiotics, perhaps due to a glycolytic shift or activated autophagy. In turn, simultaneous inhibition of autophagy and treatment with antibiotics largely reduced tumorigenic properties of cancer cells suggesting potential strategy for anticancer therapy. (C) 2016 Published by Elsevier Ireland Ltd.

Druh

J_imp - Článek v periodiku v databázi Web of Science

CEP obor

—

OECD FORD obor

30204 - Oncology

Projekt

—

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

Cancer letters

ISSN

0304-3835

e-ISSN

—

Svazek periodika

384

Číslo periodika v rámci svazku

JAN 1 2017

Stát vydavatele periodika

IE - Irsko

Počet stran výsledku

10

Strana od-do

60-69

Kód UT WoS článku

000389109700007

EID výsledku v databázi Scopus

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