Vitamin D and prostate cancer

Tuohimaa, Pentti; Lyakhovich, Alex; Aksenov, Nickolai; Pennanen, Pasi; Syvälä, Heimo; Lou, Yan-Ru; Ahonen, Merja; Hasan, Taina; Pasanen, Paavo; Bläuer, Merja; Manninen, Tommi; Miettinen, Susanna; Vilja, Pekka; Ylikomi, Timo

doi:10.1016/s0960-0760(00)00141-2

Cited by 53 publications

(29 citation statements)

References 23 publications

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“…As shown in Fig. 4C, 1␣,25(OH) 2 D 3 was equally effective in preventing etoposide-induced apoptosis in HeLa cells transiently transfected with either the wtVDR or the VDR119-C. 3 -It has been previously shown that 1␣,25(OH) 2 D 3 rapidly induces the phosphorylation of ERKs in murine osteoblastic calvaria cells and other cell types (13,30,31). We confirmed this observation here using the OB-6 murine bone marrow-derived osteoblastic cell line (Fig.…”

Section: The Ligand Binding Domain Of the Vdr Is Sufficient For Thementioning

confidence: 73%

Nongenotropic, Anti-Apoptotic Signaling of 1α,25(OH)2-Vitamin D3 and Analogs through the Ligand Binding Domain of the Vitamin D Receptor in Osteoblasts and Osteocytes

Vertino

Bula

Chen

et al. 2005

Journal of Biological Chemistry

100

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Changes in the birth or death of osteoblasts and/or osteoclasts represent fundamental pathophysiologic changes in most acquired metabolic bone diseases, including the osteoporosis that results from sex steroid deficiency, glucocorticoid excess, or old age (1-6). Furthermore, pharmacotherapeutics used commonly for the treatment of metabolic bone diseases exert their beneficial effects on bone by regulating the rate of birth of new osteoclasts or osteoblasts or their apoptosis (6 -8).We have recently shown that estrogens and androgens, acting via their classical nuclear receptors (ER␣, 1 ER␤, or AR), attenuate the apoptosis of several different cell types, including osteoblasts and osteocytes, by rapidly activating the Src/Shc/ ERK and phosphatidylinositol 3-kinase (PI3K) and down-regulating the JNK signaling pathways. This effect requires only the ligand binding, not the DNA binding, domain of the receptor, and, unlike its classical transcriptional action, it is eliminated by nuclear targeting of the receptor (9). Activation of ERKs leads to the rapid translocation of the kinases into the nucleus where they phosphorylate common transcription factors like Elk-1, CCAAT enhancer-binding protein-␤, and cAMPresponse element-binding protein. These transcription factors in turn up-regulate gene expression, as exemplified by the up-regulation of the early growth response-1 protein gene, an ERK/serum response element target gene. Likewise, suppression of the JNK signaling cascade by sex steroids leads to downregulation of c-Jun expression (10). We have earlier used a ligand that potently and selectively activates nongenotropic actions of the classical ER or AR and thereby activates kinases and their downstream transcription factors and target genes with only minimal effects on classical estrogen response element-mediated genotropic transcription. Furthermore, we have demonstrated that, although such classical genotropic actions of sex steroid receptors are essential for their effects on reproductive tissues, they are dispensable for their bone protective effects (2).

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Section: The Ligand Binding Domain Of the Vdr Is Sufficient For Thementioning

confidence: 73%

Nongenotropic, Anti-Apoptotic Signaling of 1α,25(OH)2-Vitamin D3 and Analogs through the Ligand Binding Domain of the Vitamin D Receptor in Osteoblasts and Osteocytes

Vertino

Bula

Chen

et al. 2005

Journal of Biological Chemistry

100

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“…The VDR belongs to the steroid and thyroid hormone receptor family of ligand-activated transcription factors (Tuohimaa et al 2001). Nuclear receptor superfamily comprise a large group of transcription factors, the functions of which, in many cases, are regulated by small, lipophilic hormonal ligands that include steroids, retinoids, vitamin D, and thyroid hormone.…”

Section: Discussionmentioning

confidence: 99%

The role of vitamin D receptor gene polymorphisms in the susceptibility to prostate cancer of a southern European population

et al. 2002

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“…This is an important finding that accounts for observations that high vitamin D status and residence at sunny latitudes are associated with lower mortality rates from cancer of the colon (42,43,(83)(84)(85), breast (5,6,43,86,87), ovary (43,46), and prostate (43,45,(88)(89)(90).…”

Section: Epidemiological Evidence: Latitude Vitamin D and Cancermentioning

confidence: 75%

The Emerging Role of Vitamin D in Cancer Risk Reduction

Garland¹,

Garland²,

Gorham³

et al. 2003

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Vitamin D and prostate cancer

Cited by 53 publications

References 23 publications

Nongenotropic, Anti-Apoptotic Signaling of 1α,25(OH)2-Vitamin D3 and Analogs through the Ligand Binding Domain of the Vitamin D Receptor in Osteoblasts and Osteocytes

Nongenotropic, Anti-Apoptotic Signaling of 1α,25(OH)2-Vitamin D3 and Analogs through the Ligand Binding Domain of the Vitamin D Receptor in Osteoblasts and Osteocytes

The role of vitamin D receptor gene polymorphisms in the susceptibility to prostate cancer of a southern European population

The Emerging Role of Vitamin D in Cancer Risk Reduction

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