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. 2021 Apr 28;22(9):4613. doi: 10.3390/ijms22094613

Table 2.

Onco-suppressors.

Channels
(ion flux) 		Expression in Cancer Cancer Type Effects on Wnt Signaling Mechanism of Action Effect on Tumorigenesis Ref.
CaCNA2D3
(Ca2+) 		Low Naso-pharyngeal carcinoma ↓Wnt signaling targets (cyclin D1, c-myc);
↓MMP7 (invasion);
↓ SNAIL (EMT)		 ↑ intracellular Ca2+ flux causes ↑ NLK protein kinase which antagonize canonical Wnt signaling Overexpression induces mitochondrial-mediated apoptosis and repression of Wnt-dependent invasion, proliferation and EMT. [56]
CaCNA2D3
(Ca2+) 		Low Glioma ↓ Wnt signaling targets (CCND1, c-myc);
↓ MMP7 (invasion);
↓ SNAIL (EMT)		 ↑ intracellular Ca2+ flux causes ↑ NLK protein kinase, which antagonize canonical Wnt signaling Overexpression induces mitochondrial-mediated apoptosis and repression of Wnt-dependent invasion, proliferation and EMT. [57]
CFTR
(Cl−) 		Low Colorectal cancer;
Gastric cancer		 ↓ Wnt signaling targets CFTR−/− Apcmin mice display ↑Wnt/β-catenin target genes (Ccnd1, CD44, Axin2, Lgr5, Mmp7, Wnt10A and Ptgs2) CFTR−/− mice developed significantly more tumors in the colon and the entire small intestine and alteration in the intestinal stem cell compartment. [58]
Kv7.1
(K+) 		Low Colorectal cancer ↑β-catenin-E-cadherin interaction Membrane depolarization prevents cytosolic β-catenin release through β-catenin-E-cadherin complex stabilization Reduced EMT, cell proliferation, and tumorigenesis [51]
Kv11.1
(K+) 		Low Breast cancer ↑β-catenin-E-cadherin interaction Membrane depolarization prevents cytosolic β-catenin release through β-catenin-E-cadherin complex stabilization GSK3-β-independent Represses metastasis formation [41]