The ketone body β-Hydroxybutyrate as a fuel source of chondrosarcoma cells.

Autor:	Vargas-López M; Laboratorio de Microbiología Molecular, Sección de Estudios de Posgrado e Investigación, ENMyH, Instituto Politécnico Nacional, Mexico City, 07320, Mexico., Quiroz-Vicente CA; Laboratorio de Microbiología Molecular, Sección de Estudios de Posgrado e Investigación, ENMyH, Instituto Politécnico Nacional, Mexico City, 07320, Mexico., Pérez-Hernández N; Laboratorio de Microbiología Molecular, Sección de Estudios de Posgrado e Investigación, ENMyH, Instituto Politécnico Nacional, Mexico City, 07320, Mexico., Gómez-Chávez F; Laboratorio de Microbiología Molecular, Sección de Estudios de Posgrado e Investigación, ENMyH, Instituto Politécnico Nacional, Mexico City, 07320, Mexico., Bañuelos-Hernández AE; Laboratorio de Microbiología Molecular, Sección de Estudios de Posgrado e Investigación, ENMyH, Instituto Politécnico Nacional, Mexico City, 07320, Mexico., Pérez-Hernández E; Laboratorio de Microbiología Molecular, Sección de Estudios de Posgrado e Investigación, ENMyH, Instituto Politécnico Nacional, Mexico City, 07320, Mexico.
Jazyk:	angličtina
Zdroj:	Heliyon [Heliyon] 2024 Apr 26; Vol. 10 (9), pp. e30212. Date of Electronic Publication: 2024 Apr 26 (Print Publication: 2024).
DOI:	10.1016/j.heliyon.2024.e30212
Abstrakt:	Chondrosarcoma (CS) is a malignant bone tumor arising from cartilage-producing cells. The conventional subtype of CS typically develops within a dense cartilaginous matrix, creating an environment deficient in oxygen and nutrients, necessitating metabolic adaptation to ensure proliferation under stress conditions. Although ketone bodies (KBs) are oxidized by extrahepatic tissue cells such as the heart and brain, specific cancer cells, including CS cells, can undergo ketolysis. In this study, we found that KBs catabolism is activated in CS cells under nutrition-deprivation conditions. Interestingly, cytosolic β-hydroxybutyrate dehydrogenase 2 (BDH2), rather than mitochondrial BDH1, is expressed in these cells, indicating a specific metabolic adaptation for ketolysis in this bone tumor. The addition of the KB, β-Hydroxybutyrate (β-HB) in serum-starved CS cells re-induced the expression of BDH2, along with the key ketolytic enzyme 3-oxoacid CoA-transferase 1 (OXCT1) and monocarboxylate transporter-1 (MCT1). Additionally, internal β-HB production was quantified in supplied and starved cells, suggesting that CS cells are also capable of ketogenesis alongside ketolysis. These findings unveil a novel metabolic adaptation wherein nutrition-deprived CS cells utilize KBs for energy supply and proliferation. Competing Interests: The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper. (© 2024 Published by Elsevier Ltd.)
Databáze:	MEDLINE
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