Vitamin D supplementation and clinical outcomes in cancer survivorship

Griffin, Niamh; Dowling, Maura

doi:10.12968/bjon.2018.27.19.1121

Cited by 13 publications

(11 citation statements)

References 36 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Radiotherapy is one of the most effective and frequently used tumor treatments, however, both the radioresistance of tumors and the damage caused to healthy tissues nearby tumors under high-dose ionizing radiation, limit the use of radiotherapy. Natural and synthetic vitamin D compounds have been proven as anticancer agents ( Larriba and Munoz, 2005 ; Pervin et al., 2013 ; Feldman et al., 2014 ; Griffin and Dowling, 2018 ) . It has been reported that vitamin D and vitamin D analogs radiosensitized breast cancer and lung cancer cells through altering the nature of the autophagy, converting it from a protective form to a cytotoxic form in vitro ( Sundaram and Gewirtz, 1999 ; Demasters et al., 2006 ; Bristol et al., 2012 ) .…”

Section: Discussionmentioning

confidence: 99%

“…Several clinical studies and experimental studies support that 1α dihydroxyvitamin D [1α,25(OH) 2 D 3 ] possesses anti-tumor actions in various cancers, such as breast-, colon-, and ovarian cancer ( Larriba and Munoz, 2005 ; Pervin et al., 2013 ; Feldman et al., 2014 ; Griffin and Dowling, 2018 ). Additionally, low 25(OH)D serum was associated with higher ovarian cancer susceptibility and a poor prognosis for patients with lung cancer ( Ong et al., 2016 ; Akiba et al., 2018 ).…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

1α,25(OH)2D3 Radiosensitizes Cancer Cells by Activating the NADPH/ROS Pathway

Nie

et al. 2020

Front. Pharmacol.

View full text Add to dashboard Cite

The radioresistance of tumors affect the outcome of radiotherapy. Accumulating data suggest that 1a,25(OH) 2 D 3 is a potential anti-oncogenic molecule in various cancers. In the present study, we investigated the radiosensitive effects and underlying mechanisms of 1a,25(OH) 2 D 3 in vitro and in vivo. We found that 1a,25(OH) 2 D 3 enhanced the radiosensitivity of lung cancer and ovarian cancer cells by promoting the NADPH oxidase-ROS-apoptosis axis. Compared to the group that only received radiation, the survival fraction and selfrenewal capacity of cancer cells treated with a combination of 1a,25(OH) 2 D 3 and radiation were decreased. Both apoptosis and ROS were significantly increased in the combination group compared with the radiation only group. Moreover, N-acetyl-L-cysteine, a scavenger of intracellular ROS, reversed the apoptosis and ROS induced by 1a,25(OH) 2 D 3 , indicating that 1a,25(OH) 2 D 3 enhanced the radiosensitivity of cancer cells in vitro by promoting ROSinduced apoptosis. Moreover, our results demonstrated that 1a,25(OH) 2 D 3 promoted the ROS level via activating NADPH oxidase complexes, NOX4, p22 phox , and p47 phox. In addition, knockdown of the vitamin D receptor (VDR) abolished the radiosensitization of 1a,25(OH) 2 D 3 , which confirmed that 1a,25(OH) 2 D 3 radiosensitized tumor cells that depend on VDR. Similarly, our study also evidenced that vitamin D 3 enhanced the radiosensitivity of cancer cells in vivo and extended the overall survival of mice with tumors. In summary, these results demonstrate that 1a,25(OH) 2 D 3 enhances the radiosensitivity depending on VDR and activates the NADPH oxidase-ROS-apoptosis axis. Our findings suggest that 1a,25 (OH) 2 D 3 in combination with radiation enhances lung and ovarian cell radiosensitivity, potentially providing a novel combination therapeutic strategy.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

1α,25(OH)2D3 Radiosensitizes Cancer Cells by Activating the NADPH/ROS Pathway

Nie

et al. 2020

Front. Pharmacol.

View full text Add to dashboard Cite

show abstract

“…There is also still a lack of evidence for public health recommendation for using vitamin D for patients with breast cancer, and vitamin D status is recognized as an important parameter when antiestrogen treatment causes joint pain and AI-associated arthralgia or aggravates osteoporosis [15]. Many clinical studies investigating the role of vitamin D intake during breast cancer treatment are inconclusive and have often ignored the fact that other vitamin D metabolites, in addition to the most frequently analysed, i.e., 25(OH)D 3 or 1,25(OH) 2 D 3 , arise in the body after vitamin D supplementation and some of these metabolites are active [13,[49][50][51][52][53]. As shown by A. Verma et al, together with vitamin D metabolites such as (24R)-24,25(OH) 2 D 3 , different estrogen receptor isoforms should also be considered; thus, their response to vitamin D metabolites (and probably even analogs) differs from the classical ERα (66 kDa)-mediated pathway [13].…”

Section: Cell Linementioning

confidence: 99%

Vitamin D Compounds PRI-2191 and PRI-2205 Enhance Anastrozole Activity in Human Breast Cancer Models

Filip‐Psurska

Psurski

Anisiewicz

et al. 2021

IJMS

View full text Add to dashboard Cite

1,25-Dihydroxycholecalciferol, the hormonally active vitamin D3 metabolite, is known to exhibit therapeutic effects against breast cancer, mainly by lowering the expression of estrogen receptors and aromatase activity. Previously, the safety of the vitamin D active metabolite (24R)-1,24-dihydroxycholecalciferol (PRI-2191) and 1,25(OH)2D3 analog PRI-2205 was tested, and the in vitro activity of these analogs against different cancer cell lines was studied. We determined the effect of the two vitamin D compounds on anastrozole (An) activity against breast cancer based on antiproliferative activity, ELISA, flow cytometry, enzyme inhibition potency, PCR, and xenograft study. Both the vitamin D active metabolite and synthetic analog regulated the growth of not only estrogen receptor-positive cells (T47D and MCF-7, in vitro and in vivo), but also hormone-independent cancer cells such as SKBR-3 (HER-2-positive) and MDA-MB-231 (triple-negative), despite their relatively low VDR expression. Combined with An, PRI-2191 and PRI-2205 significantly inhibited the tumor growth of MCF-7 cells. Potentiation of the antitumor activity in combined treatment of MCF-7 tumor-bearing mice is related to the reduced activity of aromatase by both An (enzyme inhibition) and vitamin D compounds (switched off/decreased aromatase gene expression, decreased expression of other genes related to estrogen signaling) and by regulation of the expression of the estrogen receptor ERα and VDR.

show abstract

“…There are no uniform global guidelines on what vitamin D doses and serum concentrations should be considered as a target in the group of patients after breast cancer treatment. The National Comprehensive Cancer Network recommends that cancer patients should maintain 25(OH)D concentration above 30 ng/mL [56]. The American Cancer Society/American Society of Clinical Oncology recommends vitamin D supplementation in patients with breast cancer starting from the age of 50 at a dose of 600-1000 IU/day [22]; in turn, ESMO recommends higher daily doses of vitamin D in this group of patients, amounting to 1000-2000 IU/day [23].…”

Section: Discussionmentioning

confidence: 99%

Effect of Selected Factors on the Serum 25(OH)D Concentration in Women Treated for Breast Cancer

et al. 2021

View full text Add to dashboard Cite

Maintaining an optimal vitamin D concentration reduces the risk of recurrence and extends survival time in patients after breast cancer treatment. Data on vitamin D deficiency among Polish women after breast cancer therapy are limited. Thus, the aim of the study was the analysis of vitamin D status in post-mastectomy patients, considering such factors as seasons, social habits, vitamin D supplementation and its measurements. The study involved 94 women after breast cancer treatment. Serum vitamin D concentration was measured, and a questionnaire, gathering demographic and clinical data regarding cancer, diet, exposure to sun radiation, and knowledge of recommendations on vitamin D supplementation, was delivered twice, in both winter and in summer. The control group consisted of 94 age-matched women with no oncological history. In women after breast cancer treatment, 25-hydroxyvitamin D (25(OH)D) deficiency was much more frequent than in the general population. Only about half of the patients supplemented vitamin D at the beginning of the study. After the first test and the issuing of recommendations on vitamin D supplementation, the percentage of vitamin D supplemented patients increased by about 30% in study groups. The average dose of supplement also increased. None of the women that were not supplementing vitamin D and were tested again in winter had optimal 25(OH)D concentration. It was concluded that vitamin deficiency is common in women treated for breast cancer. Medical advising about vitamin D supplementation and monitoring of 25(OH)D concentration should be improved.

show abstract

Vitamin D supplementation and clinical outcomes in cancer survivorship

Cited by 13 publications

References 36 publications

1α,25(OH)2D3 Radiosensitizes Cancer Cells by Activating the NADPH/ROS Pathway

1α,25(OH)2D3 Radiosensitizes Cancer Cells by Activating the NADPH/ROS Pathway

Vitamin D Compounds PRI-2191 and PRI-2205 Enhance Anastrozole Activity in Human Breast Cancer Models

Effect of Selected Factors on the Serum 25(OH)D Concentration in Women Treated for Breast Cancer

Contact Info

Product

Resources

About