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Vitamin D in Triple-Negative and BRCA1-Deficient Breast Cancer—Implications for Pathogenesis and Therapy

1
Department of Molecular Genetics, Faculty of Biology and Environmental Protection, University of Lodz, 90-236 Lodz, Poland
2
Department of Orthodontics, Medical University of Lodz, 92-216 Lodz, Poland
3
Department of Clinical Nutrition and Gastroenterological Diagnostics, Medical University of Lodz, 90-647 Lodz, Poland
4
Department of Pediatric Dentistry, Medical University of Lodz, 92-216 Lodz, Poland
5
Department of Neurology, Polish Mother Memorial Hospital Research Institute, 93-338 Lodz, Poland
*
Author to whom correspondence should be addressed.
Int. J. Mol. Sci. 2020, 21(10), 3670; https://doi.org/10.3390/ijms21103670
Received: 7 May 2020 / Revised: 21 May 2020 / Accepted: 22 May 2020 / Published: 23 May 2020
(This article belongs to the Special Issue Breast Cancer: From Pathophysiology to Novel Therapeutic Approaches)
Several studies show that triple-negative breast cancer (TNBC) patients have the lowest vitamin D concentration among all breast cancer types, suggesting that this vitamin may induce a protective effect against TNBC. This effect of the active metabolite of vitamin D, 1α,25-dihydroxyvitamin D3 (1,25(OH)2D), can be attributed to its potential to modulate proliferation, differentiation, apoptosis, inflammation, angiogenesis, invasion and metastasis and is supported by many in vitro and animal studies, but its exact mechanism is poorly known. In a fraction of TNBCs that harbor mutations that cause the loss of function of the DNA repair-associated breast cancer type 1 susceptibility (BRCA1) gene, 1,25(OH)2D may induce protective effects by activating its receptor and inactivating cathepsin L-mediated degradation of tumor protein P53 binding protein 1 (TP53BP1), preventing deficiency in DNA double-strand break repair and contributing to genome stability. Similar effects can be induced by the interaction of 1,25(OH)2D with proteins of the growth arrest and DNA damage-inducible 45 (GADD45) family. Further studies on TNBC cell lines with exact molecular characteristics and clinical trials with well-defined cases are needed to determine the mechanism of action of vitamin D in TNBC to assess its preventive and therapeutic potential. View Full-Text
Keywords: vitamin D; triple-negative breast cancer; BRCA1; genomic stability; DNA repair vitamin D; triple-negative breast cancer; BRCA1; genomic stability; DNA repair
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MDPI and ACS Style

Blasiak, J.; Pawlowska, E.; Chojnacki, J.; Szczepanska, J.; Fila, M.; Chojnacki, C. Vitamin D in Triple-Negative and BRCA1-Deficient Breast Cancer—Implications for Pathogenesis and Therapy. Int. J. Mol. Sci. 2020, 21, 3670. https://doi.org/10.3390/ijms21103670

AMA Style

Blasiak J, Pawlowska E, Chojnacki J, Szczepanska J, Fila M, Chojnacki C. Vitamin D in Triple-Negative and BRCA1-Deficient Breast Cancer—Implications for Pathogenesis and Therapy. International Journal of Molecular Sciences. 2020; 21(10):3670. https://doi.org/10.3390/ijms21103670

Chicago/Turabian Style

Blasiak, Janusz; Pawlowska, Elzbieta; Chojnacki, Jan; Szczepanska, Joanna; Fila, Michal; Chojnacki, Cezary. 2020. "Vitamin D in Triple-Negative and BRCA1-Deficient Breast Cancer—Implications for Pathogenesis and Therapy" Int. J. Mol. Sci. 21, no. 10: 3670. https://doi.org/10.3390/ijms21103670

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