Abstract
Calcium is a key regulator of many physiological processes that are perturbed in cancer, such as migration, proliferation and apoptosis. The proteins STIM and Orai mediate store-operated calcium entry (SOCE), the main pathway for calcium entry in non-excitable cells. Changes in the expression and function of STIM and Orai have been found in a range of cancer types and thus implicated in disease progression. Here we discuss the role of STIM, Orai and the SOCE pathway in the progression of melanoma and explore how the heterogeneous nature of melanoma may explain the lack of consensus in the field regarding the role of SOCE in the progression of this disease.
Highlights
Ultraviolet (UV) radiation can lead to DNA damage by causing adjacent thymine base pairs to form pyrimidine dimers (Goodsell, 2001)
Once melanoma enters the vertical growth phase, the cells infiltrate the dermis and metastasize, 5-year survival rate falls to 15%
It is known that when Wnt5a is upregulated, protein kinase C (PKC) activity is elevated (Dissanayake and Weeraratna, 2008). We found this elevated PKC activity was apparently responsible for the reduction in store-operated calcium entry (SOCE) due to Orai1 phosphorylation, a process previously demonstrated to negatively regulate the channel in vitro (Kawasaki et al, 2010)
Summary
Calcium is a key regulator of many physiological processes that are perturbed in cancer, such as migration, proliferation and apoptosis. The proteins STIM and Orai mediate store-operated calcium entry (SOCE), the main pathway for calcium entry in non-excitable cells. Changes in the expression and function of STIM and Orai have been found in a range of cancer types and implicated in disease progression. We discuss the role of STIM, Orai and the SOCE pathway in the progression of melanoma and explore how the heterogeneous nature of melanoma may explain the lack of consensus in the field regarding the role of SOCE in the progression of this disease
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