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. Author manuscript; available in PMC: 2012 May 1.
Published in final edited form as: Cancer Prev Res (Phila). 2011 Mar 24;4(5):744–751. doi: 10.1158/1940-6207.CAPR-10-0285

Fig. 1.

Fig. 1

Vitamin D3 is a potent inhibitor of cellular proliferation and Gli1 mRNA (n = 3 experiments). (A) Cellular proliferation studies were conducted in a BCC cell line (ASZ), non-tumorigenic keratinocytes (C5N), and a medulloblastoma cell line (Med1) incubated for 48 h with cyclopamine (CPN) versus 1,25(OH)2D and vitamin D3. Mean±SEM, *P < 0.01 compared to C5N. (B) Cellular proliferation was assayed in BCC cell lines (ASZ, BSZ, CSZ) and non-tumorigenic keratinocytes (C5N) 48 h after treatment. Mean±SEM, *P < 0.01 compared to C5N. (C) 24-hydroxylase mRNA relative expression in ASZ cells treated with 7DHC (10 µM), 25(OH)D (10 µM), 1,25(OH)2D (0.1 µM), vitamin D3 (10 µM), and CPN (10 µM) at 24 and 48 h. Mean±SEM, *P < 0.01 compared to control (DMSO or EtOH). (D) Gli1 mRNA relative expression in ASZ cells treated with 7DHC (10 µM), 25(OH)D (10 µM), 1,25(OH)2D (0.1 µM), vitamin D3 (10 µM), and CPN (10 µM) at 24 and 48 h. Mean±SEM, *P < 0.01 compared to control (DMSO or EtOH).

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