A metabolic switch in proteasome inhibitor-resistant multiple
myeloma ensures higher mitochondrial metabolism, protein
folding and sphingomyelin synthesis

J 2019

A metabolic switch in proteasome inhibitor-resistant multiple myeloma ensures higher mitochondrial metabolism, protein folding and sphingomyelin synthesis

BESSE, Lenka, Andrej BESSE, Max MENDEZ-LOPEZ, Kateřina VAŠÍČKOVÁ, Miroslava SEDLÁČKOVÁ et. al.

Základní údaje

Originální název

A metabolic switch in proteasome inhibitor-resistant multiple myeloma ensures higher mitochondrial metabolism, protein folding and sphingomyelin synthesis

Autoři

BESSE, Lenka (756 Švýcarsko, garant), Andrej BESSE (756 Švýcarsko), Max MENDEZ-LOPEZ (756 Švýcarsko), Kateřina VAŠÍČKOVÁ (203 Česká republika, domácí), Miroslava SEDLÁČKOVÁ (203 Česká republika, domácí), Petr VAŇHARA (203 Česká republika, domácí), Marianne KRAUS (756 Švýcarsko), Jurgen BADER (756 Švýcarsko), Renan B. FERREIRA (840 Spojené státy), Ronald K. CASTELLANO (840 Spojené státy), Brian K. LAW (840 Spojené státy) a Christoph DRIESSEN (756 Švýcarsko)

Vydání

Haematologica, PAVIA, FERRATA STORTI FOUNDATION, 2019, 0390-6078

Další údaje

Jazyk

angličtina

Typ výsledku

Článek v odborném periodiku

Obor

30205 Hematology

Stát vydavatele

Itálie

Utajení

není předmětem státního či obchodního tajemství

Odkazy

URL

Impakt faktor

Impact factor: 7.116

Kód RIV

RIV/00216224:14110/19:00110883

Organizační jednotka

Lékařská fakulta

DOI

http://dx.doi.org/10.3324/haematol.2018.207704

UT WoS

000483996100008

Klíčová slova anglicky

metabolic switch; proteasome inhibitor; multiple myeloma

Štítky

14110517, rivok

Příznaky

Mezinárodní význam, Recenzováno

Změněno: 7. 10. 2019 09:30, Mgr. Tereza Miškechová

Anotace

V originále

Proteasome inhibitors (PI) have evolved as the central backbone of treatment for multiple myeloma (MM), with first-in-class bortezomib and second- and third-generation PI, carfilzomib and ixazomib, having been approved for this indication. Proteasome inhibition disrupts the unfolded protein response to resolve excessive endoplasmic reticulum stress, but also leads to massive metabolic changes manifested by the induction of amino acid biosynthesis, an anti-oxidant response, lipogenesis and an increase in protein folding. In this sense, PI represent a unique class of drugs targeting cancer cell metabolism by affecting the balance between protein biosynthesis, folding and destruction. However, the adaptive changes in MM cell metabolism may provide the basis of resistance to PI, as high glycolytic activity or rewiring glucose metabolism is associated with bortezomib resistance in MM.

Citovat

BESSE, Lenka, Andrej BESSE, Max MENDEZ-LOPEZ, Kateřina VAŠÍČKOVÁ, Miroslava SEDLÁČKOVÁ, Petr VAŇHARA, Marianne KRAUS, Jurgen BADER, Renan B. FERREIRA, Ronald K. CASTELLANO, Brian K. LAW a Christoph DRIESSEN. A metabolic switch in proteasome inhibitor-resistant multiple myeloma ensures higher mitochondrial metabolism, protein folding and sphingomyelin synthesis. Haematologica. PAVIA: FERRATA STORTI FOUNDATION, 2019, roč. 104, č. 9, s. 415-419. ISSN 0390-6078. Dostupné z: https://dx.doi.org/10.3324/haematol.2018.207704.

@article{1566639,
   author = {Besse, Lenka and Besse, Andrej and MendezandLopez, Max and Vašíčková, Kateřina and Sedláčková, Miroslava and Vaňhara, Petr and Kraus, Marianne and Bader, Jurgen and Ferreira, Renan B. and Castellano, Ronald K. and Law, Brian K. and Driessen, Christoph},
   article_location = {PAVIA},
   article_number = {9},
   doi = {http://dx.doi.org/10.3324/haematol.2018.207704},
   keywords = {metabolic switch; proteasome inhibitor; multiple myeloma},
   language = {eng},
   issn = {0390-6078},
   journal = {Haematologica},
   title = {A metabolic switch in proteasome inhibitor-resistant multiple myeloma ensures higher mitochondrial metabolism, protein folding and sphingomyelin synthesis},
   url = {http://dx.doi.org/10.3324/haematol.2018.207704},
   volume = {104},
   year = {2019}
}

TY  - JOUR
ID  - 1566639
AU  - Besse, Lenka - Besse, Andrej - Mendez-Lopez, Max - Vašíčková, Kateřina - Sedláčková, Miroslava - Vaňhara, Petr - Kraus, Marianne - Bader, Jurgen - Ferreira, Renan B. - Castellano, Ronald K. - Law, Brian K. - Driessen, Christoph
PY  - 2019
TI  - A metabolic switch in proteasome inhibitor-resistant multiple myeloma ensures higher mitochondrial metabolism, protein folding and sphingomyelin synthesis
JF  - Haematologica
VL  - 104
IS  - 9
SP  - 415-419
EP  - 415-419
PB  - FERRATA STORTI FOUNDATION
SN  - 03906078
KW  - metabolic switch
KW  - proteasome inhibitor
KW  - multiple myeloma
UR  - http://dx.doi.org/10.3324/haematol.2018.207704
L2  - http://dx.doi.org/10.3324/haematol.2018.207704
N2  - Proteasome inhibitors (PI) have evolved as the central backbone of treatment for multiple myeloma (MM), with first-in-class bortezomib and second- and third-generation PI, carfilzomib and ixazomib, having been approved for this indication. Proteasome inhibition disrupts the unfolded protein response to resolve excessive endoplasmic reticulum stress, but also leads to massive metabolic changes manifested by the induction of amino acid biosynthesis, an anti-oxidant response, lipogenesis and an increase in protein folding. In this sense, PI represent a unique class of drugs targeting cancer cell metabolism by affecting the balance between protein biosynthesis, folding and destruction. However, the adaptive changes in MM cell metabolism may provide the basis of resistance to PI, as high glycolytic activity or rewiring glucose metabolism is associated with bortezomib resistance in MM.
ER  -

BESSE, Lenka, Andrej BESSE, Max MENDEZ-LOPEZ, Kateřina VAŠÍČKOVÁ, Miroslava SEDLÁČKOVÁ, Petr VAŇHARA, Marianne KRAUS, Jurgen BADER, Renan B. FERREIRA, Ronald K. CASTELLANO, Brian K. LAW a Christoph DRIESSEN. A metabolic switch in proteasome inhibitor-resistant multiple myeloma ensures higher mitochondrial metabolism, protein folding and sphingomyelin synthesis. \textit{Haematologica}. PAVIA: FERRATA STORTI FOUNDATION, 2019, roč.~104, č.~9, s.~415-419. ISSN~0390-6078. Dostupné z: https://dx.doi.org/10.3324/haematol.2018.207704.

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