TY - JOUR T1 - Zinc Inhibits Cadherin 1 Expression Induced by 1α,25-Dihydroxyvitamin D<sub>3</sub> in Colon Cancer Cells JF - Anticancer Research JO - Anticancer Res SP - 5453 LP - 5459 DO - 10.21873/anticanres.15357 VL - 41 IS - 11 AU - MICHIYASU ISHIZAWA AU - AYAKO HIRAYU AU - MAKOTO MAKISHIMA Y1 - 2021/11/01 UR - http://ar.iiarjournals.org/content/41/11/5453.abstract N2 - Background: Zinc is a mineral that is essential for biological molecules, such as transcription factors, and is involved in the maintenance of intestinal homeostasis. Vitamin D signaling is mediated by vitamin D receptor (VDR) activated by 1α,25-dihydroxyvitamin D3 [1,25(OH)2D3] and is also important in intestinal functions, such as calcium absorption and epithelial barrier maintenance. However, the crosstalk between vitamin D signaling and zinc signaling in intestinal cells remains poorly understood. Materials and Methods: Colon cancer SW480 and HCT116 cells were treated with zinc chloride (ZnCl2) with/without 1,25(OH)2D3. Expression of zinc-inducible genes [metallothionein 1A (MT1A) and MT2A] and VDR target genes [cytochrome P450 family 24 subfamily A member 1 (CYP24A1), transient receptor potential cation channel subfamily V member 6 (TRPV6) and cadherin 1 (CDH1)] was examined. Results: Treatment of cells with ZnCl2 effectively induced MT1A and MT2A mRNA expression, and interestingly suppressed mRNA expression of CDH1, which was induced by 1,25(OH)2D3 in both cell lines. ZnCl2 also reduced the CDH1 protein level in HCT116 cells. Conclusion: Zinc signaling suppresses VDR-induced expression of CDH1. ER -