Chronic moderate ethanol intake differentially regulates vitamin D hydroxylases gene expression in kidneys and xenografted breast cancer cells in female mice

Autor: David Ordaz-Rosado, María de Jesús Ibarra-Sánchez, David Barrera, Nancy Santos-Martínez, Galia Lara-Sotelo, José Esparza-López, Fernando Larrea, Andrea Olmos-Ortiz, Euclides Avila, Sofía López, Rocío García-Becerra, Ali Halhali, Lorenza Díaz, Janice García-Quiroz
Rok vydání: 2016
Předmět:
0301 basic medicine
medicine.medical_specialty
Calcitriol
Alcohol Drinking
Endocrinology
Diabetes and Metabolism

Clinical Biochemistry
Mice
Nude

Breast Neoplasms
Biology
Kidney
Biochemistry
vitamin D deficiency
Gene Expression Regulation
Enzymologic

03 medical and health sciences
Basal (phylogenetics)
Mice
0302 clinical medicine
Endocrinology
Breast cancer
CYP24A1
Downregulation and upregulation
Internal medicine
polycyclic compounds
medicine
Vitamin D and neurology
Animals
Humans
Vitamin D3 24-Hydroxylase
Molecular Biology
Calcifediol
25-Hydroxyvitamin D3 1-alpha-Hydroxylase
Ethanol
Cell Biology
Vitamins
medicine.disease
Gene Expression Regulation
Neoplastic

030104 developmental biology
030220 oncology & carcinogenesis
Cancer cell
Molecular Medicine
lipids (amino acids
peptides
and proteins)

Female
medicine.drug
Zdroj: The Journal of steroid biochemistry and molecular biology. 173
ISSN: 1879-1220
Popis: Factors affecting vitamin D metabolism may preclude anti-carcinogenic effects of its active metabolite calcitriol. Chronic ethanol consumption is an etiological factor for breast cancer that affects vitamin D metabolism; however, the mechanisms underlying this causal association have not been fully clarified. Using a murine model, we examined the effects of chronic moderate ethanol intake on tumoral and renal CYP27B1 and CYP24A1 gene expression, the enzymes involved in calcitriol synthesis and inactivation, respectively. Ethanol (5% w/v) was administered to 25-hydroxyvitamin D3-treated or control mice during one month. Afterwards, human breast cancer cells were xenografted and treatments continued another month. Ethanol intake decreased renal Cyp27b1 while increased tumoral CYP24A1 gene expression.Treatment with 25-hydroxyvitamin D3 significantly stimulated CYP27B1 in tumors of non-alcohol-drinking mice, while increased both renal and tumoral CYP24A1. Coadministration of ethanol and 25-hydroxyvitamin D3 reduced in 60% renal 25-hydroxyvitamin D3-dependent Cyp24a1 upregulation (P
Databáze: OpenAIRE