BRIEF COMMUNICATION: Growth Control of Human Colon Cancer Cells by Vitamin D and Calcium In Vitro

Cross, Heide S.; Pavelka, Margit; Slavík, Jan; Peterlik, Meinrad

doi:10.1093/jnci/84.17.1355

Cited by 95 publications

(42 citation statements)

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“…Pancreatic cancer is poorly influenced by chemotherapy (Jeekel, 1994) (Reichel et al, 1989;Cross et al, 1992;Bollag and Holdener, 1992;Gudas, 1992 (Harant et al, 1993), breast cancer cell lines (Roman et al, 1992), myeloma cells and leukaemic cells (Lutzky et al, 1994;Dore et al, 1993). There is no correlation between biological effects of retinoids and degree of receptor expression (van-der Leede et al, 1993;Lutzky et al, 1994), which is consistent with our results.…”

Section: Discussionmentioning

confidence: 99%

“…EB 1089 is a potent inhibitor of proliferation of breast cancer cells in vitro and in vivo (Colston et al, 1992). Other vitamin D analogues have been developed that significantly inhibit the growth of human colon cancer cells in vitro (Cross et al, 1992;Shabahang et al, 1994). These analogues reduce the growth rate twice as effectively as does dihydroxyvitamin D3 (Shabahang et al, 1994).…”

Section: Discussionmentioning

confidence: 99%

“…The biologically active form of vitamin D, 1,25-dihydroxyvitamin D3 25(OH) D3] exerts effects unrelated to calcium homeostasis such as inhibiting proliferation of cancer cells (Cross et al, 1992). Receptors for vitamin D are present in a variety of cancer cells, including pancreatic adenocarcinoma (Reichel et al, 1989).…”

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confidence: 99%

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Growth-inhibitory effects of vitamin D analogues and retinoids on human pancreatic cancer cells

Zugmaier

Jager²,

Grage³

et al. 1996

Br J Cancer

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Summary Retinoids and vitamin D are important factors that regulate cellular growth and differentiation. An additive growth-inhibitory effect of retinoids and vitamin D analogues has been demonstrated for human myeloma, leukaemic and breast cancer cells. We set out to study the effects of the vitamin D analogue EB1089 and the retinoids all-trans-and 9-cis-retinoic acid on the human pancreatic adenocarcinoma cell lines Capan 1 and Capan 2 and the undifferentiated pancreatic carcinoma cell line Hs766T. The cell lines investigated expressed vitamin D receptor, retinoic acid receptor (RAR)-a and y as determined by polymerase chain reaction after reverse transcription. RAR-f, was expressed only in Hs766T cells. Addition of all-trans-retinoic acid increased the amount of RAR-a mRNA in the three cell lines and induced RAR-,B mRNA in Capan 1 and Capan 2 cells. All-trans-retinoic acid at a concentration of 10 nM inhibited the growth of Capan 1 and Capan 2 cells by 40% relative to controls. 9-cis-Retinoic acid was less effective. Neither all-trans-retinoic acid nor 9-cisretinoic acid affected the growth of Hs766T cells. EB1089, if added alone to the cells, did not significantly inhibit growth. However, the combination of 1 nM EB1089 with 10 nM all-trans-retinoic acid exerted a growthinhibitory effect of 90% in Capan 1 cells and of 70% in Capan 2 cells. Our data suggest that vitamin D analogues together with retinoids inhibit the growth of human pancreatic cancer cells. However, in vivo studies are necessary to examine the potential use of retinoids and vitamin D analogues on pancreatic cancer.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Growth-inhibitory effects of vitamin D analogues and retinoids on human pancreatic cancer cells

Zugmaier

Jager²,

Grage³

et al. 1996

Br J Cancer

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“…Experimental studies suggest that vitamin D may inhibit cell proliferation (Shabahang et al, 1994;Cross et al, 1992;Wallach et al, 1966;Taniyama et al, 2000). The cell growth inhibitory properties of the vitamin appear to be related to the concentrations of vitamin D receptors on the cell surface rather than vitamin D concentrations.…”

Section: Vitamin Dmentioning

confidence: 99%

Dairy products and colorectal cancer. A review of possible mechanisms and epidemiological evidence

2003

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Objectives: This review provides an overview of the principal hypotheses and epidemiological evidence of the possible links between colorectal cancer and intake of milk and=or dairy products. Methods: The first section outlines the main hypotheses about the possible effect of calcium, vitamin D, fats and other milk components. The possible role of acid lactic bateria in fermented products is also discussed. The second section is a summary of the published epidemiological evidence. The results on milk, cheese and yoghurt are summarized using a meta-analytical approach. The results of studies on calcium and vitamin D are briefly described. Results: Case -control studies are heterogeneous and, on average, do not provide evidence of association between total intake of total dairy products, milk, cheese or yoghurt and colorectal cancer risk. The average result from cohort studies support the hypothesis of a protective effect of total dairy products (odds ratio (OR): 0.62; 95% confidence interval (CI): 0.52 -0.74; P heterogeneity test: 0.93) and for milk (OR: 0.80; 95% CI: 0.68 -0.95; P heterogeneity: 0.77). No association was found between cheese (OR: 1.10; 95% CI: 0.88 -1.36; P heterogeneity: 0.55) or yoghurt (OR: 1.03; 95% CI: 0.83 -1.28; P heterogeneity: 0.69) in cohort studies. Conclusions: Cohort studies consistently found a protective effect of total dairy products and milk intake, but the evidence is not supported by case -control studies. No relationship was found with cheese or yoghurt intake. As the number of cohort studies is still limited, their results need to be confirmed by other prospective studies.

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“…Tamoxifen apparently acts as a membrane antioxidant by structural mimicry of cholesterol (and ergosterol) thus enabling it to act in a similar way to stabilise the membrane against lipid peroxidation [13,14,17,18]. It is interesting, therefore, that Vitamin D, its active metabolite and also synthetic analogues have been reported to have anticancer activity [19][20][21][22][23][24]. Cholecalciferol, its me- tabolite 1,25-dihydroxycholecalciferol and 7-dehydrocholesterol are derived from and structurally related to cholesterol, whereas ergosterol is the parent compound of ergocalciferol and this led us to investigate their antioxidant abilities.…”

Section: Introductionmentioning

confidence: 99%

Vitamin D is a membrane antioxidant Ability to inhibit iron‐dependent lipid peroxidation in liposomes compared to cholesterol, ergosterol and tamoxifen and relevance to anticancer action

1993

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Vitamin D is a membrane antioxidant: thus Vitamin D 3 (cholecalciferol) and its active metabolite 1,25-dihydroxycholecalciferol and also Vitamin D 2 (ergocalciferol) and 7-dehydrocholesterol (pro-Vitamin D3) all inhibited iron-dependent liposomal lipid peroxidation. Cholecalciferol, 1,25-dihydroxycholecalciferol and ergocalciferol were all of similar effectiveness as inhibitors of lipid peroxidation but were less effective than 7-dehydrocholesterol; this was a better inhibitor of lipid peroxidation than cholesterol, though not ergosterol. The structural basis for the antioxidant ability of these Vitamin D compounds is considered in terms of their molecular relationship to cholesterol and ergosterol. Furthermore, the antioxidant ability of Vitamin D is compared to that of the anticancer drug tamoxifen and its 4-hydroxy metabolite (structural mimics of cholesterol) and discussed in relation to the anticancer action of this vitamin.

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BRIEF COMMUNICATION: Growth Control of Human Colon Cancer Cells by Vitamin D and Calcium In Vitro

Cited by 95 publications

References 0 publications

Growth-inhibitory effects of vitamin D analogues and retinoids on human pancreatic cancer cells

Growth-inhibitory effects of vitamin D analogues and retinoids on human pancreatic cancer cells

Dairy products and colorectal cancer. A review of possible mechanisms and epidemiological evidence

Vitamin D is a membrane antioxidant Ability to inhibit iron‐dependent lipid peroxidation in liposomes compared to cholesterol, ergosterol and tamoxifen and relevance to anticancer action

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