In recent decades cancer emerged as one of the leading causes of death in the developed countries, with some types of cancer contributing to the top 10 causes of death on the list of the World Health Organization. Carcinogenesis, a malignant transformation causing formation of tumors in normal tissues, is associated with changes in the cell cycle caused by suppression of signaling pathways leading to cell death and facilitation of those enhancing proliferation. Further progression of cancer, during which benign tumors acquire more aggressive phenotypes, is characterized by metastatic dissemination through the body driven by augmented motility and invasiveness of cancer cells. All these processes are associated with alterations in calcium homeostasis in cancer cells, which promote their proliferation, motility and invasion, and dissuade cell death or cell cycle arrest. Remodeling of store-operated calcium entry (SOCE), one of the major pathways regulating intracellular Ca^2 + concentration ([Ca^2 +]_i), manifests a key event in many of these processes. This review systematizes current knowledge on the mechanisms recruiting SOCE—related proteins in carcinogenesis and cancer progression.

近几十年来，癌症成为发达国家的主要死因之一，其中某些类型的癌症在世界卫生组织的名单上排名前 10 位。致癌作用是一种导致正常组织中形成肿瘤的恶性转化，它与细胞周期的变化有关，这种变化是由抑制导致细胞死亡的信号通路和促进那些促进增殖的信号通路引起的。癌症的进一步进展，在此期间良性肿瘤获得更具侵袭性的表型，其特征在于通过增强的运动性和癌细胞的侵袭性驱动的通过身体的转移性传播。所有这些过程都与癌细胞中钙稳态的改变有关，从而促进它们的增殖、运动和侵袭，并阻止细胞死亡或细胞周期停滞。钙库操作钙进入（SOCE）的重塑，调节细胞内钙的主要途径之一^{2  +}浓度（[Ca ^{2  +} ] _i）在许多这些过程中表现出关键事件。这篇综述系统化了目前关于在致癌作用和癌症进展中招募 SOCE 相关蛋白的机制的知识。