IP3 Receptor-Mediated Calcium Signaling and Its Role in Autophagy in Cancer.

摘要: Calcium ions (Ca2+) play a complex role in orchestrating diverse cellular processes including cell death and survival. To trigger signaling cascades, intracellular Ca2+ is shuffled between the cytoplasm major stores, endoplasmic reticulum (ER), mitochondria, lysosomes. A key control of signals attributed to inositol 1,4,5-trisphosphate (IP3) receptors (IP3Rs), main Ca2+-release channels ER. IP3Rs can transfer thereby stimulating core metabolic pathways, but also increasing apoptosis sensitivity inhibiting basal autophagy. On other hand, IP3-induced release enhances autophagy flux by providing cytosolic required execute upon various stresses, nutrient starvation, chemical mTOR inhibition or drug treatment. Similarly, are able amplify from lysosomes therefore impact autophagic response lysosomal activation. Furthermore, indirect modulation through may be achieved controlling SERCA pumps Considering cancer development progression as well anticancer therapies, it becomes clear that important fully understand IP3R its context this disease. In cells addicted ER-mitochondria fueling, lead via mechanisms involving enhanced mitotic catastrophe. Moreover, targets several oncogenes tumor suppressors functional loss these genes, occurring many types, result modified transport mitochondria level flux. IP3R-mediated upregulation protect some against NK cells-induced killing. The involvement regulation both directly biology contribute molecular basis pathology.