SCI SIGNAL: What do cancer cells with oxidizing phosphorylation defects survive?

!---- existing studies have shown that spontaneous Ca2-plus signal conduction from the Ca2-plus release channel within InsP3R cells to the mitochondria is essential for the production of optimal oxyped phosphorylation (OXPHOS) and ATPin cells with OXPHOS defects, reductive carnitination replaces oxidation metabolism to maintain the reduction equivalent and the number of metabolic precursorsto study the role of mitochondrial Ca2 plus ingesting in regulating biological energy in these cells, the researchers used oxPHOS cells with function and OXPHOS defectsinhibition of InsP3R activity or mitochondrial Ca2 plus intake increases the abundance of alpha-ketone diacid (alphaKG) and the NAD-NADH ratio, indicating that the constituent endosome(ER)-mitochondrial Ca2-plus transfer promotes the optimal activity of alpha-kgdease (alpha KGDH)reducemidrop mitochondrial Ca2 plus inhibits alpha KGDH activity and increases NAD plus, thereby inducing SIRT1-dependent autophagy, a phenomenon that is present in OXPHOS-competent and OXPHOS-defective cellsautophagy flux in OXPHOS-competent cells promotes cell survival, while autophagy flux is impaired in OXPHOS-defective cells due to inhibition of autophagy-lysosome fusionin OXPHOS defective cells, the inhibition of alpha KGDH and the loss of autophagy flux lead to cell death in response to the interruption of the constituent flux from Ca2 plus to mitochondrialthese results show that mitochondria play a fundamental role in maintaining the bioenergy balance of OXPHOS sound cells and OXPHOS defective cells, in which Ca2 plus plays a key role in regulating alpha KGDH activityinhibition of Ca2-plus metastasis from ER to mitochondria may be a common treatment for cancer cells, regardless of their OXPHOS status.