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

Table 3.

Onco-channels.

Channels
(ion flux)
Expression in Cancer Cancer Type Effects on Wnt Signaling Mechanism of Action Effect on Tumorigenesis Ref.
Trp5
(non-selective Ca2+ cation channel)
High Colorectal cancer ↑Wnt5a, ↑ Wnt signaling targets (cyclin D1 and c-myc) ↑ Trp5 increase Ca2+ influx in the cell, which induces ↑Wnt5a and ↑ nuclear β-catenin levels Channel upregulation reduces colorectal cancer differentiation and stemness through Ca2+-Wnt5a [59]
Trp5
(non-selective Ca2+ cation channel)
High Colorectal cancer β-catenin stabilization Reduction in levels of the channels reduces Ca2+ influx lowering β-catenin stability Silencing of the channel reduces colorectal cancer tumorigenesis and ameliorates 5-Fluorouracil chemoresistance [55]
TRPM4
(non-selective Ca2+ cation channel)
High Prostate cancer ↑β-catenin stabilization ↑ GSK3β and AKT1 phospho-inactive form through Ca2+ flux Tumor proliferation and progression [60]
TRPV2
(non-selective Ca2+ cation channel)
High Esophageal squamous cell carcinoma ↑ Wnt signaling Increased Ca2+ flux results in ↑ Wnt signaling. The precise mechanism of action still to be determined. Promotes proliferation, invasion, and angiogenesis [61]
BKCa
(K+)
High Breast cancer ↑β-catenin stabilization Modulation of transmembrane depolarization regulates phospho-AKT and, in turn, β-catenin stability Pharmacological inhibition of the channel (Ibtx) reduces anchorage-dependent growth and tumorigenesis [62]