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Cell-specific modulation of mitochondrial respiration and metabolism by the pro-apoptotic Bcl-2 family members Bax and Bak

D. Sovilj, CD. Kelemen, S. Dvorakova, R. Zobalova, H. Raabova, J. Kriska, Z. Hermanova, T. Knotek, M. Anderova, P. Klener, V. Filimonenko, J. Neuzil, L. Andera

. 2024 ; 29 (3-4) : 424-438. [pub] 20231124

Language English Country Netherlands

Document type Journal Article

Persistent link   https://www.medvik.cz/link/bmc24006616

Grant support
GA19-08772S Czech Science Foundation
GX21-04607X Czech Science Foundation
86652036 Institute of Biotechnology
LM2023050 Ministry of Education, Youth and Sports of the Czech Republic
L200392251 Czech Academy of Sciences
NU21-03-00386 Ministry of Health of the Czech Republic

E-resources Online Full text

NLK ProQuest Central from 1997-01-01 to 1 year ago
Medline Complete (EBSCOhost) from 2000-02-01 to 1 year ago
Health & Medicine (ProQuest) from 1997-01-01 to 1 year ago

Links

PubMed 38001340
DOI 10.1007/s10495-023-01917-2
Knihovny.cz E-resources

Proteins from the Bcl-2 family play an essential role in the regulation of apoptosis. However, they also possess cell death-unrelated activities that are less well understood. This prompted us to study apoptosis-unrelated activities of the Bax and Bak, pro-apoptotic members of the Bcl-2 family. We prepared Bax/Bak-deficient human cancer cells of different origin and found that while respiration in the glioblastoma U87 Bax/Bak-deficient cells was greatly enhanced, respiration of Bax/Bak-deficient B lymphoma HBL-2 cells was slightly suppressed. Bax/Bak-deficient U87 cells also proliferated faster in culture, formed tumours more rapidly in mice, and showed modulation of metabolism with a considerably increased NAD+/NADH ratio. Follow-up analyses documented increased/decreased expression of mitochondria-encoded subunits of respiratory complexes and stabilization/destabilization of the mitochondrial transcription elongation factor TEFM in Bax/Bak-deficient U87 and HBL-2 cells, respectively. TEFM downregulation using shRNAs attenuated mitochondrial respiration in Bax/Bak-deficient U87 as well as in parental HBL-2 cells. We propose that (post)translational regulation of TEFM levels in Bax/Bak-deficient cells modulates levels of subunits of mitochondrial respiratory complexes that, in turn, contribute to respiration and the accompanying changes in metabolism and proliferation in these cells.

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