Abstract
Constitutive calcium signaling in cancer cells drives tumor proliferation and metastasis. Secretory Pathway Ca2+-ATPases (SPCA) were highly upregulated in breast cancer derived cell lines and human breast tumors. Depletion of SPCA in human breast adenocarcinoma cells attenuated basal Ca2+ levels and downstream cell proliferation, anchorage-independent growth and tumor formation in mice. Contrary to its known role in Golgi Ca2+ sequestration, SPCA overexpression increased cytosolic Ca2+ by activation of the store-operated Ca2+ channels. However, SPCA mediated Ca2+ influx was independent of Ca2+ stores or sensors and not dependent on its transport ATPase activity, revealing a new signaling paradigm.
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