BET inhibitors (BETi) influence oxidative phosphorylation metabolism by affecting mitochondrial dynamics leading to alterations in apoptotic pathways in triple‐negative breast cancer (TNBC) cells DOI Creative Commons
Teresa Rossi, Egidio Iorio, Mattea Chirico

et al.

Cell Proliferation, Journal Year: 2024, Volume and Issue: 57(12)

Published: Sept. 2, 2024

Repressing BET proteins' function using bromodomain inhibitors (BETi) has been shown to elicit antitumor effects by regulating the transcription of genes downstream BRD4. We previously showed that BETi promoted cell death triple-negative breast cancer (TNBC) cells. Here, we proved induce altered mitochondrial dynamics fitness in TNBC cells falling death. demonstrated treatment downregulated expression BCL-2, and proteins involved fission increased fused mitochondria. Impaired affected oxidative phosphorylation (OXPHOS) inducing OXPHOS-related genes, SDHa ATP5a, Consistently, amount DNA membrane potential (∆Ψm) BETi-treated compared control Lastly, combination with Metformin reduced growth. Our results indicate OXPHOS metabolism support proliferation represent novel targets

Language: Английский

Tumor energy metabolism: implications for therapeutic targets DOI Creative Commons

Youwu Hu,

Wanqing Liu,

WanDi Fang

et al.

Molecular Biomedicine, Journal Year: 2024, Volume and Issue: 5(1)

Published: Nov. 29, 2024

Abstract Tumor energy metabolism plays a crucial role in the occurrence, progression, and drug resistance of tumors. The study tumor has gradually become an emerging field treatment. Recent studies have shown that epigenetic regulation is closely linked to metabolism, influencing metabolic remodeling biological traits cells. This review focuses on primary pathways explores therapeutic strategies target these pathways. It covers key areas such as glycolysis, Warburg effect, mitochondrial function, oxidative phosphorylation, adaptability Additionally, this article examines regulator SWI/SNF complex specifically its interactions with glucose, lipids, amino acids. Summarizing aimed at pathways, including inhibitors mitochondrial-targeted drugs, exploitation vulnerabilities, recent developments related complexes potential targets. clinical significance, challenges, future directions research are discussed, overcome resistance, combination therapy, application new technologies.

Language: Английский

Citations

7
BET inhibitors (BETi) influence oxidative phosphorylation metabolism by affecting mitochondrial dynamics leading to alterations in apoptotic pathways in triple‐negative breast cancer (TNBC) cells DOI Creative Commons
Teresa Rossi, Egidio Iorio, Mattea Chirico

et al.

Cell Proliferation, Journal Year: 2024, Volume and Issue: 57(12)

Published: Sept. 2, 2024

Repressing BET proteins' function using bromodomain inhibitors (BETi) has been shown to elicit antitumor effects by regulating the transcription of genes downstream BRD4. We previously showed that BETi promoted cell death triple-negative breast cancer (TNBC) cells. Here, we proved induce altered mitochondrial dynamics fitness in TNBC cells falling death. demonstrated treatment downregulated expression BCL-2, and proteins involved fission increased fused mitochondria. Impaired affected oxidative phosphorylation (OXPHOS) inducing OXPHOS-related genes, SDHa ATP5a, Consistently, amount DNA membrane potential (∆Ψm) BETi-treated compared control Lastly, combination with Metformin reduced growth. Our results indicate OXPHOS metabolism support proliferation represent novel targets

Language: Английский

Citations

2