Triple-negative breast cancer (TNBC) is a subtype of invasive cancer in breast with the symptoms of unfavourable prognosis and limited targeted treatment options. Evidence of changes in the metabolic status of TNBC, characterised by increased glycolysis, mitochondrial oxidative phosphorylation, as well as production and utilization of tricarboxylic acid cycle intermediates.
Investigate the proteins altered in cryptotanshinone treated MDA-MB-231 cells and explore the key pathways and specific molecular markers involved in cryptotanshinone treatment.
We use unlabeled quantitative proteomics to gain insight into the anticancer mechanism of cryptotanshinone on MDA-MB231 triple negative breast cancer cells. And flow cytometry was used to detect apoptosis and changes in cell mitochondrial membrane potential.
We show that inhibiting the expression of electron transport chain complex proteins, also inhibits mitochondrial oxidative phosphorylation. Additionally, down-regulation of the ribosime biogenesis pathway was found to inhibit cell metabolism.
In summary, results show that cryptotanshinone can trigger rapid and irreversible apoptosis in MDA-MB-231 cells through effectively inhibiting cell metabolism.