Vitamin D signalling pathways in cancer: potential for anticancer therapeutics View Full Text


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Article Info

DATE

2007-09

AUTHORS

Kristin K. Deeb, Donald L. Trump, Candace S. Johnson

ABSTRACT

Key PointsEpidemiological studies point to a relationship between vitamin D deficiency and cancer risk.Alterations in vitamin D receptor expression, and in the synthesis (25-hydroxylase and 1α-hydroxylase) and catabolism (24-hydroxylase) of vitamin D metabolites are involved in the growth regulation of tumours; thus, compromising 1α,25(OH)2D3 (also known as calcitriol; the active metabolite of vitamin D signalling) sensitivity and 1α,25(OH)2D3 signalling.The antiproliferative effects of 1α,25(OH)2D3 have been demonstrated in various tumour types, as determined by preclinical trials.The anti-tumour effects of 1α,25(OH)2D3 involve mechanisms that are associated with G0/G1 arrest, differentiation, induction of apoptosis and modulating different signalling pathways in tumour cells, as well as inhibiting tumour angiogenesis.Glucocorticoids potentiate the anti-tumour effects of 1α,25(OH)2D3 and decrease 1α,25(OH)2D3-induced hypercalcemia. 1α,25(OH)2D3 also potentiates the anti-tumour effects of many chemotherapeutic agents such as platinum analogues, taxanes and DNA-intercalating agents.Given that the major vitamin D catabolizing enzyme, CYP24A1 (24-hydroxylase), is often amplified and overexpressed in tumour cells, agents that inhibit this enzyme can potentiate 1α,25(OH)2D3 anti-tumour effects.Preclinical data indicate that maximal anti-tumour effects are seen with pharmacological doses of 1α,25(OH)2D3, and can be safely achieved in animals using a high-dose, intermittent schedule of administration. Some clinical trial data indicates that 1α,25(OH)2D3 is well-tolerated in cancer patients within a proper dosing schedule.Data support the hypothesis that vitamin D compounds may have an important role in cancer therapy and prevention, and merit further investigation. More... »

PAGES

684-700

References to SciGraph publications

  • 2005-07-11. 1α,25-Dihydroxyvitamin D3 regulates the expression of Id1 and Id2 genes and the angiogenic phenotype of human colon carcinoma cells in ONCOGENE
  • 2003. Analysis of the Vitamin D System in Cervical Carcinomas, Breast Cancer and Ovarian Cancer in VITAMIN D ANALOGS IN CANCER PREVENTION AND THERAPY
  • 2005-09-23. Expression of VDR and CYP24A1 mRNA in human tumors in CANCER CHEMOTHERAPY AND PHARMACOLOGY
  • 2003-07-15. A phase II study of the vitamin D analogue Seocalcitol in patients with inoperable hepatocellular carcinoma in BRITISH JOURNAL OF CANCER
  • 2004-04-12. Analysis of the vitamin D system in basal cell carcinomas (BCCs) in LABORATORY INVESTIGATION
  • 2002-12-28. Pharmacokinetics of high‐dose oral calcitriol: Results from a phase 1 trial of calcitriol and paclitaxel in CLINICAL PHARMACOLOGY & THERAPEUTICS
  • 1993-02. Two nuclear signalling pathways for vitamin D in NATURE
  • 2004-08-09. Altered SMRT levels disrupt vitamin D3 receptor signalling in prostate cancer cells in ONCOGENE
  • 2003-01. Nongenomic actions of steroid hormones in NATURE REVIEWS MOLECULAR CELL BIOLOGY
  • 2000-11. Prostate cancer risk and prediagnostic serum 25-hydroxyvitamin D levels (Finland) in CANCER CAUSES & CONTROL
  • 1998-07. A phase I study of the vitamin D analogue EB 1089 in patients with advanced breast and colorectal cancer in BRITISH JOURNAL OF CANCER
  • 2006-10-26. Phase I study of weekly DN-101, a new formulation of calcitriol, in patients with cancer in CANCER CHEMOTHERAPY AND PHARMACOLOGY
  • 1997-08. Mice lacking the vitamin D receptor exhibit impaired bone formation, uterine hypoplasia and growth retardation after weaning in NATURE GENETICS
  • 2000-06. Quantitative mapping of amplicon structure by array CGH identifies CYP24 as a candidate oncogene in NATURE GENETICS
  • 2001-05. The vitamin D3 analog, ILX-23-7553, enhances the response to Adriamycin and irradiation in MCF-7 breast tumor cells in CANCER CHEMOTHERAPY AND PHARMACOLOGY
  • 1999-01. Combined effect of vitamin D3 analogs and paclitaxel on the growth of MCF-7 breast cancer cells in vivo in BREAST CANCER RESEARCH AND TREATMENT
  • 2004-08-22. The transcription factor SNAIL represses vitamin D receptor expression and responsiveness in human colon cancer in NATURE MEDICINE
  • 2002-02-26. A phase II trial of the vitamin D analogue Seocalcitol (EB1089) in patients with inoperable pancreatic cancer in BRITISH JOURNAL OF CANCER
  • Journal

    TITLE

    Nature Reviews Cancer

    ISSUE

    9

    VOLUME

    7

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  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1038/nrc2196

    DOI

    http://dx.doi.org/10.1038/nrc2196

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1021224284

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/17721433


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    40 schema:description Key PointsEpidemiological studies point to a relationship between vitamin D deficiency and cancer risk.Alterations in vitamin D receptor expression, and in the synthesis (25-hydroxylase and 1α-hydroxylase) and catabolism (24-hydroxylase) of vitamin D metabolites are involved in the growth regulation of tumours; thus, compromising 1α,25(OH)2D3 (also known as calcitriol; the active metabolite of vitamin D signalling) sensitivity and 1α,25(OH)2D3 signalling.The antiproliferative effects of 1α,25(OH)2D3 have been demonstrated in various tumour types, as determined by preclinical trials.The anti-tumour effects of 1α,25(OH)2D3 involve mechanisms that are associated with G0/G1 arrest, differentiation, induction of apoptosis and modulating different signalling pathways in tumour cells, as well as inhibiting tumour angiogenesis.Glucocorticoids potentiate the anti-tumour effects of 1α,25(OH)2D3 and decrease 1α,25(OH)2D3-induced hypercalcemia. 1α,25(OH)2D3 also potentiates the anti-tumour effects of many chemotherapeutic agents such as platinum analogues, taxanes and DNA-intercalating agents.Given that the major vitamin D catabolizing enzyme, CYP24A1 (24-hydroxylase), is often amplified and overexpressed in tumour cells, agents that inhibit this enzyme can potentiate 1α,25(OH)2D3 anti-tumour effects.Preclinical data indicate that maximal anti-tumour effects are seen with pharmacological doses of 1α,25(OH)2D3, and can be safely achieved in animals using a high-dose, intermittent schedule of administration. Some clinical trial data indicates that 1α,25(OH)2D3 is well-tolerated in cancer patients within a proper dosing schedule.Data support the hypothesis that vitamin D compounds may have an important role in cancer therapy and prevention, and merit further investigation.
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