Store-Operated Ca2+ Entry as a Prostate Cancer Biomarker — a Riddle with Perspectives

Abstract

Purpose of Review Store-operated calcium entry (SOCE) is dysregulated in prostate cancer, contributing to increased cel-lular migration and proliferation and preventing cancer cell apoptosis. We here summarize findings on gene expression levels and functions of SOCE components, stromal interaction molecules (STIM1 and STIM2), and members of the Orai protein family (Orai1, 2, and 3) in prostate cancer. Moreover, we introduce new research models that promise to provide insights into whether dysregulated SOCE signaling has clinically relevant implications in terms of increasing the migration and invasion of prostate cancer cells. Recent Findings Recent reports on Orai1 and Orai3 expres-sion levels and function were in part controversial probably due to the heterogeneous nature of prostate cancer. Lately, in prostate cancer cells, transient receptor melastatin 4 channel was shown to alter SOCE and play a role in migration and proliferation. We specifically highlight new cancer research models: a subpopulation of cells that show tumor initiation and metastatic potential in mice and zebrafish models. Summary This review focuses on SOCE component dysreg-ulation in prostate cancer and analyzes several preclinical, cellular, and animal cancer research models.