Suppression of Ca signaling enhances melanoma progression.

The role of store-operated Ca entry (SOCE) in melanoma metastasis is highly controversial. To address this, we here examined UV-dependent metastasis, revealing a critical role for SOCE suppression in melanoma progression. UV-induced cholesterol biosynthesis was critical for UV-induced SOCE suppression and subsequent metastasis, although SOCE suppression alone was both necessary and sufficient for metastasis to occur.

Ca as a therapeutic target in cancer.

Ca is a ubiquitous and dynamic second messenger molecule that is induced by many factors including receptor activation, environmental factors, and voltage, leading to pleiotropic effects on cell function including changes in migration, metabolism and transcription. As such, it is not surprising that aberrant regulation of Ca signals can lead to pathological phenotypes, including cancer progression. However, given the highly context-specific nature of Ca-dependent changes in cell function, delineation of its role in cancer has been a challenge.