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View full-text article in PMC

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

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© 2020 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).

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Proposed mechanisms of calcium-dependent Epithelial to Mesenchymal Transition (EMT), migration and invasion in prostate cancer (PCa) cells. Upregulation of intracellular calcium levels dependent on K+ channel (small conductance calcium-activated potassium channel 3) SK3, Transient receptor potential (TRP) and Orai channels overactivate transcription factor Zinc finger E-box-binding homeobox 1 (Zeb1) triggering the expression of EMT genes. EMT genes are also activated by ATP-stimulated P2X7 channel. Invasion of PCa cells is mediated by upregulation of metalloproteases (MMPs) and cathepsin B via TRPV2 and TRPC6-dependent increase of cytosolic calcium levels by a constitutive mechanism. MMPs are also increased by psoriasin. Prostate cell migration is promoted by actin remodeling via calcium receptor (CasR)/calpain/filamin and Wnt5a/Calcium/Calmodulin-Dependent Kinase (CAMK)II pathways. Decreased annexin II and increased Stromal-interacting molecule 1 (STIM1)/Akt kinase activation lead to enhanced cell migration as well. Decreased TRPM8 expression decrease in late stages of androgen-insensitive PCA and is associated with increased cell migration. Arrows indicate upregulated expression or activity (↑) and downregulated expression or activity (↓). Crosses (X) indicate inhibition. Blue filled arrows indicate stimulation. ER: Endoplasmic reticulum.