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. 2020 Apr 25;12(5):1071. doi: 10.3390/cancers12051071

Figure 2.

Figure 2

Proposed mechanisms of calcium-dependent proliferation in prostate cancer (PCa) cells. Upregulation of T-Type Calcium Channels (TTCC) increases the proliferative signals Akt kinase, mammalian target of rapamycin (mTOR), cyclin-dependent kinase 4 (CDK4) and cyclin D1. Transient receptor potential (TRP)V6 (TRPV6) increase proliferation via calcium-dependent activation of Nuclear factor of activated T-cells (NFAT). TRPM4 induces proliferation through activation of calcium-dependent Akt and catenin/Tcf/Lef signaling. Piezo1, TRPC6 and TRPM7 contribute to increased calcium cytosolic levels. Nuclear localization of TRPM2 as well as sarco/endoplasmic reticulum calcium ATPase (SERCA) also promote PCa cell proliferation. Upregulation of muscarinic acetylcholine receptor M3 (CHRM3) induces Akt, glycolysis, lipogenesis, and androgen receptor (AR) re-activation via activation of Calcium/Calmodulin-Dependent Kinase Kinase (CAMKK) causing cell proliferation. Proliferation is also triggered by overactivation of Akt and Extracellular-regulated (ERK) kinases by S100 proteins and by downregulation of regucalcin. Arrows indicate upregulated expression or activity (↑) and downregulated expression or activity (↓). Blue filled arrows indicate stimulation. ER: Endoplasmic reticulum.