Comparison of VDR Expression and Blood Vitamin D 1.25 (OH)2 Level between Cervical Cancer Patients and Normal Women
Background: Vitamin D and its receptor (VDR) play a crucial role in the development of gynecological cancers. This study aims to evaluate the VDR expression and blood vitamin D 1.25 (OH)2 levels in cervical cancer patients and healthy women.
Methods: This is a cross-sectional study. In vitro quantitative examination (ELISA) was used for the measurement of vitamin D 1.25 (OH)2 and Sandwich-ELISA was applied for quantitative determination in vitro concentration of Human VDR in serum.
Results: The number of research subjects consisting of 20 cervical cancer patients based on clinical and histopathological results and 20 women without cervical cancer based on clinical and pap smear results. The mean vitamin D 1.25 (OH)2 levels in the cervical cancer group of 209.23 ± 71.476 pg/mL were significantly lower than in the group of normal women of 339.79 ± 139.003 pg/mL (P=.001). The mean VDR expression in the cervical cancer group of 5.38 ± 5.478 ng/mL was significantly higher than the group of normal women of 1.89 ± 1.657 ng/mL (P=.018). The best cut-off value for vitamin D levels is 239.25 pg/mL (sensitivity 70% and specificity 75%). The cut-off value for VDR expression is 2.23 ng/mL (sensitivity 60% and specificity 75%). Low vitamin D levels increase the risk of cervical cancer incidence by 2.7 times greater, and an increase in VDR expression increases the risk of cervical cancer incidence 2 times greater.
Conclusions: The study results indicated a higher expression of VDR and lower levels of vitamin D 1.25 (OH)2 in cervical cancer compared to normal women. Low levels of vitamin D increase the risk of cervical cancer incidence by 2.7 times greater, and higher VDR expression increases the risk of cervical cancer incidence 2 times greater.
Bray F, Ferlay J, Soerjomataram I, Siegel RL, Torre LA, Jemal A. Global cancer statistics 2018: GLOBOCAN estimates of incidence and mortality worldwide for 36 cancers in 185 countries. CA Cancer J Clin [Internet]. 2018;68(6):394–424. Available from: http://www.ncbi.nlm.nih.gov/pubmed/30207593.
Attar R, Gasparri ML, Halim TA, Hamwi D Al, Ucak I, Fayyaz S, et al. Legacy of Vitamin D : Role of Vitamin D in Prevention of Gynecological Cancers. In: Farooqi AA, Ismail M, editors. Molecular Oncology: Underlying Mechanisms and Translational Advancements.
Islamabad, Pakistan: Springer; 2017. p. 1–14.
Lappe JM, Travers-gustafson D, Davies KM, Recker RR, Heaney RP. Vitamin D and calcium supplementation reduces cancer risk : results of a randomized trial 1, 2. Am J Clin Nutr. 2007;85:1586-91.
Deeb KK, Trump DL, Johnson CS. Vitamin D signaling pathways in cancer: Potential for anticancer therapeutics. Nat Rev Cancer. 2007;7(9):684-700.
Özgü E, Yılmaz N, Ba E, Güngör T, Erkaya S, Yakut Hİ. Could 25-OH vitamin D deficiency be a reason for HPV infection persistence in cervical premalignant lesions?. J Exp Ther Oncol. 2016;11(3):177-80.
Yan L, Gu Y, Luan T, Miao M, Jiang L, Liu Y, et al. Associations between serum vitamin D and the risk of female reproductive tumors: A meta-analysis with trial sequential analysis. Medicine (Baltimore). 2018;97(15):e0360.
Hosono S, Matsuo K, Kajiyama H, Hirose K, Suzuki T, Kawase T, et al. Association between dietary calcium and vitamin D intake and cervical carcinogenesis among Japanese women. Eur J Clin Nutr. 2010;64(4):400-9.
Wang G, Lei L, Zhao X, Zhang J, Zhou M, Nan K. Calcitriol Inhibits Cervical Cancer Cell Proliferation Through Downregulation of HCCR1 Expression. Oncol Res. 2014;22(77):301-9.
Avila E, García-becerra R, Rodríguez-rasgado JA, Díaz L, Ordaz-rosado D, Zügel U, et al. Calcitriol Down-regulates Human Ether à go-go 1 Potassium Channel Expression in Cervical Cancer Cells. Anticancer Res. 2010(7);30:2667-72.
Deuster E, Jeschke U, Ye Y, Mahner S, Czogalla B. Vitamin D and VDR in gynecological cancers-A systematic review. Int J Mol Sci. 2017;18(11):2328.
Vaughan-Shaw PG, O’Sullivan F, Farrington SM, Theodoratou E, Campbell H, Dunlop MG, et al. The impact of Vitamin D pathway genetic variation and circulating 25-hydroxyVitamin D on cancer outcome: Systematic review and meta-Analysis. Br J Cancer. 2017;116(8):1095-110.
Serrano D, Gnagnarella P, Raimondi S, Gandini S. Meta-analysis on Vitamin D receptor and cancer risk: Focus on the role of TaqI, ApaI, and Cdx2 polymorphisms. Eur J Cancer Prev. 2016;25(1):85–96.
Reichrath JR, Rafi L, Muller SM, Mink D, Reitnauer K, Tilgen W, et al. Immunohistochemical analysis of 1, 25- dihydroxy vitamin D 3 receptor in cervical carcinoma. Histochem J. 1998;30(8):561-7.
Avila E, García-Becerra R, Rodríguez-Rasgado JA, Díaz L, Ordaz-Rosado D, Zügel U, et al. Calcitriol down-regulates human ether à go-go 1 potassium channel expression in cervical cancer cells. Anticancer Res. 2010;30(7):2667–72.
Tuohimaa P. Vitamin D, aging, and cancer. Nutr Rev. 2008;66(10 Suppl 2):S147-52.
Article MetricsAbstract view : 53 times
PDF - 27 times
- There are currently no refbacks.
Copyright (c) 2020 Indonesian Journal of Cancer
This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License.