Induction of apoptosis and inhibition of prostate and breast cancer growth by BGP-15, a new calcipotriene-derived vitamin D3 analog

Berkovich, Liron; Ben‐Shabat, Shimon; Sintov, Amnon

doi:10.1097/cad.0b013e328337f3e9

Cited by 10 publications

(3 citation statements)

References 33 publications

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“…Several other cell studies show 1,25(OH) 2 D or its analogs can induce apoptosis in prostate cancer cells (29, 30). These phenomena have also been seen in animal studies after treatment with vitamin D analogs, e.g.…”

Section: Discussionmentioning

confidence: 98%

Dietary Vitamin D and Vitamin D Receptor Level Modulate Epithelial Cell Proliferation and Apoptosis in the Prostate

Kovalenko

Zhang

et al. 2011

Cancer Prevention Research

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Low vitamin D (VD) status may increase prostate cancer risk but experimental evidence for this relationship is modest. We tested whether low VD status or VD receptor (VDR) deletion influences prostate epithelial cell (PEC) biology using intact mice, castrated mice, or castrated mice treated with testosterone propionate (TP, 2.5 mg/kg BW). PEC proliferation (Ki-67 staining) and apoptosis (TUNEL method) were determined in the anterior prostate (AP). In study 1, wild-type (WT) and TgAPT121 mice (a model of prostate intraepithelial neoplasia) were fed diets with 25, 200 (reference diet), or 10000 IU VD/kg diet (as vitamin D3) prior to castration/repletion. Serum 25 hydroxyvitamin D levels were 26, 78, and 237 nmol/L in the three diet groups, respectively. Castration reduced proliferation and increased apoptosis in the AP while TP reversed these effects. Low VD diet increased proliferation in WT (+82%) and TgAPT121 (+24%) mice while it suppressed apoptosis in WT (−29%) and TgAPT121 (−37%) mice. This diet also increased the severity of PIN lesions in the AP of intact TgAPT121 mice. In study 2, mice with PEC-specific VDR deletion (PEC VDR KO) were examined after castration/repletion. TUNEL staining was 60% lower in castrated PEC VDR KO mice compared to castrated WT mice. In castrated mice given TP, Ki-67 staining was 2-fold higher in PEC VDR KO compared to WT mice. Our data show that low diet VDR or VDR deletion provide a prostate environment that is permissive to early procarcinogenic events that enhance prostate cancer risk.

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Section: Discussionmentioning

confidence: 98%

Dietary Vitamin D and Vitamin D Receptor Level Modulate Epithelial Cell Proliferation and Apoptosis in the Prostate

Kovalenko

Zhang

et al. 2011

Cancer Prevention Research

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“…In vitro studies showed that this molecule may regulate cell differentiation and proliferation and exhibits growth-inhibiting effects against several human cancer cell lines including HL-60 and HL60/MX2 promyelocytic leukemia, U937 histiocytic lymphoma, MCF-7, T47D human breast cancer, HT-29 human colon cancer, and human SCC (Colston et al, 1992;Meephansan et al, 2012;Milczarek et al, 2013aMilczarek et al, , 2014. Regarding the possible mechanisms underlying the growth inhibiting and pro-differentiating effects of calcipotriol on tumor cells, in vitro studies highlighted the fact that a 20-h exposure of LNCaP prostate cancer cells and MCF-7 breast cancer cells to this analogue or to BGP-15, a new calcipotriene-derived vitamin D 3 analogue, generated procaspase-3 cleavage and ultimately, apoptosis (Berkovic et al, 2010). In addition, Wang et al (2010b) recently reported that calcipotriol significantly suppressed in vitro colon carcinoma cell invasion and enhanced the cytotoxicity of the anticancer regimen FOLFIRI (folinic acid, 5-FU, irinotecan) to cells in culture or in anchorage-independent growth.…”

Section: Calcipotriolmentioning

confidence: 99%

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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“…The vitamin D analog V decreases Bcl-2 expression in DU 145 cells [191]. Some calcitriol analogs have been shown to induce caspase-dependent apoptosis in several PCa cells [94,192]. Induction of apoptosis by calcitriol, however, appears to be cell-specific as it is not uniformly evident in all the cells that respond to calcitriol with growth inhibition.…”

Section: Apoptosismentioning

confidence: 98%