Novel pathways that contribute to the anti-proliferative and chemopreventive activities of calcitriol in prostate cancer

Krishnan, Aruna V.; Moreno, Jacqueline; Nonn, Larisa; Malloy, Peter J.; Swami, Srilatha; Peng, Linfeng; Peehl, Donna M.; Feldman, David

doi:10.1016/j.jsbmb.2006.12.051

Cited by 89 publications

(69 citation statements)

References 70 publications

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“…Likewise, a similar effect was observed by other authors on colorectal cancer cells (Schwab et al, 2007) and prostate cancer cells (Krishnan & Feldman, 2010). Nevertheless, as opposing results have been also reported on the effects of Vit D on NF-kB expression levels (Bao et al, 2010;Janjetovic et al, 2011;Krishnan et al, 2007) further studies may better define the role of NF-kB in autophagy and, consequently, the potential therapeutic impact of Vit D in modulating this phenomenon in cancer cells.…”

Section: Vit D and Autophagysupporting

confidence: 78%

“…However, a very limited number of studies have been performed to assess the role of the immune regulatory function of Vit D in cancer. In this context, Krishnan et al (2007) reported that calcitriol exhibits anti-inflammatory effects that may account for its inhibitory activity in prostate cancer. More recently, Bessler and Djaldetti (2012) showed that Vit D alters the relationship between immune and cancer cells leading to a significant decrease in the pro-inflammatory cytokines TNF-a and IL-6.…”

Section: Vit D and The Immune Systemmentioning

confidence: 99%

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Vitamin D in cancer chemoprevention

Giammanco¹,

Majo²,

Guardia

et al. 2015

Pharmaceutical Biology

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Context: There is increasing evidence that Vitamin D (Vit D) and its metabolites, besides their well-known calcium-related functions, may also exert antiproliferative, pro-differentiating, and immune modulatory effects on tumor cells in vitro and may also delay tumor growth in vivo. Objective: The aim of this review is to provide fresh insight into the most recent advances on the role of Vit D and its analogues as chemopreventive drugs in cancer therapy. Methods: A systematic review of experimental and clinical studies on Vit D and cancer was undertaken by using the major electronic health database including ISI Web of Science, Medline, PubMed, Scopus and Google Scholar. Results and conclusion: Experimental and clinical observations suggest that Vit D and its analogues may be effective in preventing the malignant transformation and/or the progression of various types of human tumors including breast cancer, prostate cancer, colorectal cancer, and some hematological malignances. These findings suggest the possibility of the clinical use of these molecules as novel potential chemopreventive and anticancer agents.

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Section: Vit D and Autophagysupporting

confidence: 78%

Section: Vit D and The Immune Systemmentioning

confidence: 99%

Vitamin D in cancer chemoprevention

Giammanco¹,

Majo²,

Guardia

et al. 2015

Pharmaceutical Biology

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“…47 49 The complexity is further revealed by the finding that 1,25(OH) 2 D 3 inhibits p38MAPK through the induction of the expression of MKP5 phosphatase in prostate cells. 50 In rat hippocampal neurons, E2 increases [Ca 2+ ] cyt by modulating L-type voltage-dependent Ca 2+ channels and this results in Src, ERK and CREB activation. 51 Curiously, Madak-Erdogan et al 18 have reported that E2 increased activated p38MAPK and JNK, but inhibitors of these two enzymes had no impact on gene regulation by either nuclear or extranuclear-activated ER in MCF-7 cells.…”

Section: Nuclear and Extranuclear Nr Effects Integratementioning

confidence: 99%

Nuclear receptors: Genomic and non-genomic effects converge

Ordóñez‐Morán¹,

Muñoz²

2009

Cell Cycle

100

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“…When bound to the vitamin D receptor, 1,25(OH) 2 D regulates more than 60 genes that exert prodifferentiating, antiproliferative, and antimetastatic effects on prostate cells through multiple mechanisms (55), including effects on cell cycle, angiogenesis (56) and downregulation of PTH-related protein expression by prostate cancer cells (57; see refs. 58, 59 for reviews).…”

Section: Pth Suppressionmentioning

confidence: 99%

Prostate Cancer, Serum Parathyroid Hormone, and the Progression of Skeletal Metastases

Schwartz

2008

Cancer Epidemiology, Biomarkers &Amp; Prevention

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Bony metastases from prostate cancer are a significant cause of morbidity and mortality. These metastases are predominantly blastic (bone-forming) and commonly cause increased serum levels of parathyroid hormone (PTH) as calcium ions are transferred from serum into blastic bone. The epidemiologic and clinical significance of secondary hyperparathyroidism in advanced prostate cancer have not been widely appreciated. Prostate cancer bony metastases show increased expression of the PTH receptor (PTH-IR) and PTH promotes the growth and invasiveness of prostate cancer cells in bone. Thus, blastic metastases appear to induce a ''vicious cycle'' in which PTH resorbs normal bone to support the growth of blastic bone. Recognition of the potential role of PTH in the progression of skeletal metastases suggests novel opportunities for prostate cancer secondary prevention. In particular, we propose that suppressing serum PTH in advanced prostate cancer may reduce morbidity by decreasing fractures and pain caused by bone resorption and may reduce mortality by retarding the progression of metastatic disease. (Cancer Epidemiol Biomarkers Prev 2008; 17(3):478 -83)

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Novel pathways that contribute to the anti-proliferative and chemopreventive activities of calcitriol in prostate cancer

Cited by 89 publications

References 70 publications

Vitamin D in cancer chemoprevention

Vitamin D in cancer chemoprevention

Nuclear receptors: Genomic and non-genomic effects converge

Prostate Cancer, Serum Parathyroid Hormone, and the Progression of Skeletal Metastases

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