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

J 2017

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

EŠNER, Milan, Dmitry GRAIFER, Matilde E. LLEONART and Alex LYAKHOVICH

Basic information

Original name

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

Authors

EŠNER, Milan (203 Czech Republic, guarantor, belonging to the institution), Dmitry GRAIFER (643 Russian Federation), Matilde E. LLEONART (724 Spain) and Alex LYAKHOVICH (643 Russian Federation)

Edition

Cancer letters, CLARE, ELSEVIER IRELAND LTD, 2017, 0304-3835

Other information

Language

English

Type of outcome

Článek v odborném periodiku

Field of Study

30204 Oncology

Country of publisher

Ireland

Confidentiality degree

není předmětem státního či obchodního tajemství

Impact factor

Impact factor: 6.491

RIV identification code

RIV/00216224:14110/17:00096272

Organization unit

Faculty of Medicine

DOI

http://dx.doi.org/10.1016/j.canlet.2016.09.023

UT WoS

000389109700007

Keywords in English

Antibiotics; Mitochondrial dysfunction; Mitochondria; Cancer; Autophagy; Mitophagy

Abstract

V originále

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.

Citovat

EŠNER, Milan, Dmitry GRAIFER, Matilde E. LLEONART and Alex LYAKHOVICH. Targeting cancer cells through antibiotics-induced mitochondrial dysfunction requires autophagy inhibition. Cancer letters. CLARE: ELSEVIER IRELAND LTD, 2017, vol. 384, JAN 1 2017, p. 60-69. ISSN 0304-3835. Available from: https://dx.doi.org/10.1016/j.canlet.2016.09.023.

@article{1375083,
   author = {Ešner, Milan and Graifer, Dmitry and Lleonart, Matilde E. and Lyakhovich, Alex},
   article_location = {CLARE},
   article_number = {JAN 1 2017},
   doi = {http://dx.doi.org/10.1016/j.canlet.2016.09.023},
   keywords = {Antibiotics; Mitochondrial dysfunction; Mitochondria; Cancer; Autophagy; Mitophagy},
   language = {eng},
   issn = {0304-3835},
   journal = {Cancer letters},
   title = {Targeting cancer cells through antibiotics-induced mitochondrial dysfunction requires autophagy inhibition},
   volume = {384},
   year = {2017}
}

TY  - JOUR
ID  - 1375083
AU  - Ešner, Milan - Graifer, Dmitry - Lleonart, Matilde E. - Lyakhovich, Alex
PY  - 2017
TI  - Targeting cancer cells through antibiotics-induced mitochondrial dysfunction requires autophagy inhibition
JF  - Cancer letters
VL  - 384
IS  - JAN 1 2017
SP  - 60-69
EP  - 60-69
PB  - ELSEVIER IRELAND LTD
SN  - 03043835
KW  - Antibiotics
KW  - Mitochondrial dysfunction
KW  - Mitochondria
KW  - Cancer
KW  - Autophagy
KW  - Mitophagy
N2  - 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.
ER  -

EŠNER, Milan, Dmitry GRAIFER, Matilde E. LLEONART and Alex LYAKHOVICH. Targeting cancer cells through antibiotics-induced mitochondrial dysfunction requires autophagy inhibition. \textit{Cancer letters}. CLARE: ELSEVIER IRELAND LTD, 2017, vol.~384, JAN 1 2017, p.~60-69. ISSN~0304-3835. Available from: https://dx.doi.org/10.1016/j.canlet.2016.09.023.

Detailed Information on Publication Record