Abstract
In normal physiology, calcium concentration is tightly regulated intracellularly and extracellularly; it acts as a versatile second messenger regulating many functional processes, such as muscle contraction, hormone secretion, cell division, apoptosis, and cell motility. Imbalance of calcium signaling in lung cancer has a significant impact on key molecular processes, including the regulation of calcium channels, pumps, calcium-binding proteins, and mitochondrial regulators. Disruption of these systems contributes to the development of the tumor process, resistance to apoptosis and activation of angiogenesis, which makes the molecules of these signaling pathways promising biomarkers for diagnostics, prognostic assessment, as well as potential targets for the development of new therapeutic approaches. Therapeutic management of calcium balance in lung cancer is considered as a promising strategy for targeted therapy.