Distinct proteomic and acylproteomic adaptations to succinate dehydrogenase loss in two cell contexts.

ABSTRACT:

Background

The tricarboxylic acid (TCA) cycle and electron transport chain (ETC) are key metabolic pathways required for cellular ATP production. While loss of components in these pathways typically impairs cell survival, such defects can paradoxically promote tumorigenesis in certain cell types. One such example is loss of succinate dehydrogenase (SDH), which functions in both the TCA cycle and as Complex II of the ETC. Deleterious mutations in SDH subunits can cause pheochromocytoma and paraganglioma (PPGL), rare hereditary neuroendocrine tumors of chromaffin cells in the adrenal gland and the nerve ganglia, respectively. Why tumor formation upon SDH loss is limited to certain tissues remains unclear. We hypothesized that the metabolic and proteomic perturbations resulting from S

SUBMITTER: Zhou SX 

PROVIDER: S-EPMC12324459 | biostudies-literature | 2025 Aug

REPOSITORIES: biostudies-literature