Sichuan University, Chengdu, China.
Int J Oral Sci. 2013 Jun;5(2):71-4. doi: 10.1038/ijos.2013.23. Epub 2013 May 10.
Recent studies in secretory pathway calcium ATPases (SPCA) revealed novel functions of SPCA2 in interacting with store-operated Ca(2+) channel Orai1 and inducing Ca(2+) influx at the cell surface. Importantly, SPCA2-mediated Ca(2+) signaling is uncoupled from its conventional role of Ca(2+)-ATPase and independent of store-operated Ca(2+) signaling pathway. SPCA2-induced store-independent Ca(2+) entry (SICE) plays essential roles in many important physiological processes, while unbalanced SICE leads to enhanced cell proliferation and tumorigenesis. Finally, we have summarized the clinical implication of SICE in oral cancer prognosis and treatment. Inhibition of SICE may be a new target for the development of cancer therapeutics.
近期的分泌途径钙 ATP 酶（SPCA）研究揭示了 SPCA2 与储存操纵的钙（Ca2+）通道 Orai1 相互作用并在细胞表面诱导 Ca2+内流的新功能。重要的是，SPCA2 介导的 Ca2+信号与传统的 Ca2+-ATP 酶作用解耦，并且独立于储存操纵的 Ca2+信号通路。SPCA2 诱导的非储存依赖性 Ca2+内流（SICE）在许多重要的生理过程中发挥着重要作用，而不平衡的 SICE 则导致细胞增殖和肿瘤形成增强。最后，我们总结了 SICE 在口腔癌预后和治疗中的临床意义。抑制 SICE 可能是癌症治疗新疗法的一个新靶点。
