VitD3, Vitamin D3: Click to Expand ⟱
Features: Promote calcium and phosphorus absorption
- Major VITAL study stated Vit D did not reduce invasive cancer, but Secondary Analysis stated reduces the incidence of metastatic cancer at diagnosis.
- Amount needed may depend on your BMI.
- Vitamin D deficiency, as determined by serum 25(OH)D concentrations of less than 30 ng/mL,
- Target achieving 80 ng/mL
- Reduces oxidative stress (ROS)
- Nrf2 plays a key role in protecting cells against oxidative stress; this is modulated by vitamin D
- Vit D supplementation may not be compatible with pro-oxidant therapy?

The minimal level is considered to be 30 ng/mL (50 nmol/L).
- One recommendation is to get your level up to around 125 ng/ml
- Chemo depletes Vitamin D levels so 10,000 IUs daily? – ask your doctor first.

After correction of vitamin D deficiency through loading doses of oral vitamin D (or safe sun exposure), adequate maintenance doses of vitamin D3 are needed. This can be achieved in approximately 90% of the adult population with vitamin D supplementation between 1000 to 4000 IU/day, 10,000 IU twice a week, or 50,000 IU twice a month [10,125]. On a population basis, such doses would allow approximately 97% of people to maintain their serum 25(OH)D concentrations above 30 ng/mL [19,126]. Others, such as persons with obesity, those with gastrointestinal disorders, and during pregnancy and lactation, are likely to require doses of 6,000 IU/day.

Vitamin D, particularly its active form 1,25-dihydroxyvitamin D (calcitriol), exerts multiple biological effects that may influence cancer development and progression.
Calcitriol has been reported to induce cell cycle arrest (often at the G0/G1 phase) and promote pro-apoptotic mechanisms in various cancer cell types.

Inhibition of Angiogenesis:
Some studies indicate that vitamin D can reduce the expression of pro-angiogenic factors, thereby potentially limiting the blood supply to tumors, which is necessary for tumor growth and metastasis.

Effects on the Wnt/β-catenin Pathway:
The Wnt/β-catenin signaling pathway, often dysregulated in several cancers (for example, colorectal cancer), may be modulated by vitamin D.
Calcitriol has been shown in some models to inhibit β-catenin signaling, which is associated with decreased cell proliferation and tumor progression.
Vitamin D may interact with other signaling pathways, including the PI3K/AKT/mTOR pathway, which is involved in cell survival and proliferation.
Scientific Papers found: Click to Expand⟱
1496- SFN,  VitD3,    Association between histone deacetylase activity and vitamin D-dependent gene expressions in relation to sulforaphane in human colorectal cancer cells
- in-vitro, CRC, Caco-2
eff↑, data suggest that colon cancer cells respond to dietary components differently under different conditions.
VDR↑, in proliferating Caco-2 cells, D + SFN (P < 0.04) increased VDR expression and decreased CYP27B1
CYP11A1↓,
HDAC↓, Histone deacetylase (HDAC) inhibitor activity was assessed using HDAC I/II assay that measured global changes in acetylation status.

115- VitD3,    Vitamin D3 triggers antitumor activity through targeting hedgehog signaling in human renal cell carcinoma Vitamin D3 Inhibits Hedgehog Signaling and Proliferation in Murine Basal Cell Carcinomas
- in-vivo, RCC, NA - in-vivo, BCC, NA
HH↓,
GLI2↓,
Shh↓,
Gli1↓,

1223- VitD3,    Vitamin D3 Treatment Influences PGE2 and TGFβ in Normal and Increased Breast Cancer Risk Women
- Trial, NA, NA
*TGF-β↑, TGFβ2 increase correlated with increase in 25(OH)D. DBP serum levels
*PGE2↓,

1313- VitD3,  MEL,    The effects of melatonin and vitamin D3 on the gene expression of BCl-2 and BAX in MCF-7 breast cancer cell line
- in-vitro, BC, MCF-7
BAX↑, upregulation of Bax gene
Bcl-2↓,
Bax:Bcl2↑, Bax/BCL-2 ratio was increased significantly
eff↑, treatment with melatonin and vitamin D3 inhibits the proliferation and induced apoptosis in breast cancer cells

1738- VitD3,    VITAL study: an incomplete picture?
- Trial, Var, NA
AntiCan↑, normal-weight individuals in the vitamin D group showed a lower cancer incidence compared to those in the placebo group
*BioAv↓, decreased bioactivity of vitamin D associated with obesity
Dose↑, 6,000-10,000 IU/day for 8 weeks, followed by maintenance therapy of 3,000-6,000 IU/day

1739- VitD3,    Effect of Vitamin D3 Supplements on Development of Advanced Cancer
- Trial, Var, NA
AntiCan↑, vitamin D3 may reduce the risk of developing advanced cancer among adults without a diagnosis of cancer at baseline; this protective effect is apparent for those who have normal but not elevated body mass index.
Dose↝, Vitamin D3 (cholecalciferol, 2000 IU/d) and marine omega-3 fatty acids (1 g/d) supplements.
Risk↓, people who took vitamin D supplements with those who took a placebo for at least 3 years; people who took vitamin D supplements had a 13% lower risk of dying from cancer than those who took a placebo
TumCP↓, , inhibition of cancer cell proliferation, and anti-inflammatory, immunomodulatory, proapoptotic, and antiangiogenic effects.
Inflam↓,
eff∅, There was no association of omega-3 fatty acid supplementation with advanced cancer, nor was there an interaction by omega-3 treatment arm

1740- VitD3,    Vitamin D and Cancer: An Historical Overview of the Epidemiology and Mechanisms
- Review, Var, NA
Risk↓, An analysis of 25(OH)D-cancer incidence rates suggests that achieving 80 ng/mL vs. 10 ng/mL would reduce cancer incidence rates by 70 ± 10%.
eff↑, In 1936, Peller reported that people who developed skin cancer from light exposure, such as from their occupation, had lower rates of internal cancers
eff↑, low rates(internal cancer) in three southwest states and high rates in approximately 15 northeast states
Risk↓, Inverse correlations were found for 11 cancers with respect to solar UVB doses for white Americans and several types of cancer for black Americans
Risk↓, It reported an 82% lower risk of breast cancer for 25(OH)D concentration >60 ng/mL versus <20 ng/mL
ChemoSen↑, Sensitization to Apoptosis, Combined Action with Chemotherapy and Radiotherapy
RadioS↑,
Cyt‑c↑, it favors the release of cytochrome C from mitochondria and the activation of caspases 3 and 9 that lead to apoptosis promoted by a variety of signals
Casp3↑,
Casp9↑,
hTERT↓, by downregulation of telomerase reverse transcriptase (hTERT) via the induction of miR-498
eff↑, In addition, 1,25-(OH)2D3 and metformin have additive/synergistic antiproliferative and proapoptotic effects in colon carcinoma and other types of cells, which are modulated but not hampered by TP53 status
E-cadherin↑, 1,25-(OH)2D3 upregulates an array of intercellular adhesion molecules that are constituents of adherens junctions and tight junctions, including E-cadherin, occludin, claudin-2 and -12, and ZO-1 and -2
CLDN2↑,
ZO-1↑,
Snail↓, 1,25-(OH)2D3 inhibits SNAIL1 and ZEB1 expression in non-small cell lung carcinoma cells
Zeb1↓,
Vim↓, vimentin downregulation
VEGF↓, 1,25-(OH)2D3 alone and more strongly in combination with cisplatin suppresses VEGF activity in ovarian cancer cells
NK cell↑, 1,25-(OH)2D3 is an enhancer of innate immune reactions against infections and tumor cells by activating the responsive cells (macrophages, natural killer (NK) cells, and neutrophils)
Risk↓, vitamin D deficiency promotes gut permeability, colon mucosa bacterial infiltration, and translocation of intestinal pathogens. These effects lead to changes in immune cell populations and gut inflammation, and cancer—an overall condition that is im
eff↑, Combination with immunotherapy

1741- VitD3,    Vitamin D Deficiency: Effects on Oxidative Stress, Epigenetics, Gene Regulation, and Aging
- Review, Var, NA
*Inflam↓, Vitamin D is one of the key controllers of systemic inflammation, oxidative stress
*antiOx↑, Vitamin D is also a potent anti-oxidant
*eff↑, Excess Sun Exposure Does Not Cause Hypervitaminosis D
*ROS↓, When vitamin D status is adequate, many of the intracellular oxidative stress-related activities are downregulated.
*NRF2↑, The intracellular Nrf2 level is inversely correlated with the accumulation of mitochondrial ROS [51,60] and the consequent escalation of oxidative stress.
*GPx↑, Vitamin D also upregulates the expression of glutathione peroxidase that converts the ROS molecule H2O2 to water
*Dose↝, adequate maintenance doses of vitamin D3 are needed. This can be achieved in approximately 90% of the adult population with vitamin D supplementation between 1000 to 4000 IU/day, 10,000 IU twice a week, or 50,000 IU twice a month
Dose↑, Others, such as persons with obesity, those with gastrointestinal disorders, and during pregnancy and lactation, are likely to require doses of 6,000 IU/day

2171- VitD3,    Vitamin D and the Immune System
- Analysis, Nor, NA
eff↑, beneficial effects of supplementing vitamin D deficient individuals with autoimmune disease may extend beyond the effects on bone and calcium homeostasis.
Dose↝, Cod liver oil, a rich source of vitamin D has also been employed as a treatment for tuberculosis as well as for general increased protection from infections
eff↝, seasonal infections varied, and were lowest in the summer and highest in the winter, the association of lower serum vitamin D levels and infection held during each season
eff↑, ll have reported an association of lower vitamin D levels and increased rates of infection
eff↑, above 40nmol

2365- VitD3,    Vitamin D Affects the Warburg Effect and Stemness Maintenance of Non- Small-Cell Lung Cancer Cells by Regulating the PI3K/AKT/mTOR Signaling Pathway
- in-vitro, Lung, A549 - in-vitro, Lung, H1975 - in-vivo, NA, NA
Glycolysis↓, vitamin D inhibited glycolysis and stemness maintenance in A549 and NCI-H1975 cells.
Warburg↓, vitamin D attenuated the expression of metabolism-related enzymes associated with the Warburg effect (GLUT1, LDHA, HK2, and PKM2).
GLUT1↓,
LDHA↓,
HK2↓,
PKM2↓,
OCT4↓, In addition, vitamin D down-regulated the expression of stemness-related genes (Oct-4, SOX-2, and Nanog) and the expression of PI3K, AKT, and mTOR.
SOX2↓,
Nanog↓,
PI3K↓,
Akt↓,
mTOR↓,

2366- VitD3,    Vitamin D3 decreases glycolysis and invasiveness, and increases cellular stiffness in breast cancer cells
- in-vitro, BC, MCF-7
Glycolysis↓, We find that VD3 treatment significantly down-regulates glycolytic enzymes and genes and decreases glucose uptake - for both lowly metastatic MCF-7 and highly metastatic MDA-MB-231 (MB231) breast cancer cells.
tumCV↓, VD3 also significantly decreases cell viability by inducing apoptosis
Apoptosis↑,
mTOR↓, consistent with decreased expression of mammalian target of rapamycin (mTOR),
AMPK↑, increases 5' adenosine monophosphate-activated protein kinase (AMPK) activation
EMT↓, presumably a consequence of reversal of the epithelial to mesenchymal transition
E-cadherin↑, increased E-cadherin, and F-actin, and reduced vimentin expression
F-actin↑,
Vim↓,

2367- VitD3,    Vitamin D activates FBP1 to block the Warburg effect and modulate blast metabolism in acute myeloid leukemia
- in-vivo, AML, NA
FBP1↑, VD3-induced FBP1 overexpression might be a novel therapeutic target to block the “Warburg Effect” to reduce energy production in AML blasts.
Warburg↓,
Glycolysis↓,
lactateProd↓, functional lactate assay showed the significant reduction of the lactate concentration in MV4–11 cells after 1,25VD3 treatment

2368- VitD3,    Vitamin D3 supplementation shapes the composition of gut microbiota and improves some obesity parameters induced by high-fat diet in mice
- in-vivo, Obesity, NA
*Weight↓, VD3 supplementation reduced body weight and the levels of TG, TC, HDL-C, TNF-α, IL-1β and LPS, and increased ZO-1 in HFD-fed mice
*TNF-α↓,
*IL1β↓,
LPS↓,
*ZO-1↑,
*GutMicro↑, increased α-diversity, reduced F/B ratio and altered microbiota composition by increasing relative abundance of Bacteroidetes, Proteobacteria, Desulfovibrio, Dehalobacterium, Odoribacter, and Parabacteroides and reducing relative abundance of Firmic

2369- VitD3,    Long Non-coding RNA MEG3 Activated by Vitamin D Suppresses Glycolysis in Colorectal Cancer via Promoting c-Myc Degradation
- in-vitro, CRC, DLD1 - in-vitro, CRC, RKO
MEG3↑, MEG3 can be activated by vitamin D and vitamin D receptor (VDR).
Glycolysis↓, overexpression of MEG3 significantly inhibited glycolysis
lactateProd↓, as well as lactate production in CRC cells
LDHA↓, inhibited c-Myc target genes involved in the glycolysis pathway such as lactate dehydrogenase A
PKM2↓, pyruvate kinase muscle 2, and hexokinase 2
HK2↓,


* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 14

Results for Effect on Cancer/Diseased Cells:
Akt↓,1,   AMPK↑,1,   AntiCan↑,2,   Apoptosis↑,1,   BAX↑,1,   Bax:Bcl2↑,1,   Bcl-2↓,1,   Casp3↑,1,   Casp9↑,1,   ChemoSen↑,1,   CLDN2↑,1,   CYP11A1↓,1,   Cyt‑c↑,1,   Dose↑,2,   Dose↝,2,   E-cadherin↑,2,   eff↑,9,   eff↝,1,   eff∅,1,   EMT↓,1,   F-actin↑,1,   FBP1↑,1,   Gli1↓,1,   GLI2↓,1,   GLUT1↓,1,   Glycolysis↓,4,   HDAC↓,1,   HH↓,1,   HK2↓,2,   hTERT↓,1,   Inflam↓,1,   lactateProd↓,2,   LDHA↓,2,   LPS↓,1,   MEG3↑,1,   mTOR↓,2,   Nanog↓,1,   NK cell↑,1,   OCT4↓,1,   PI3K↓,1,   PKM2↓,2,   RadioS↑,1,   Risk↓,5,   Shh↓,1,   Snail↓,1,   SOX2↓,1,   TumCP↓,1,   tumCV↓,1,   VDR↑,1,   VEGF↓,1,   Vim↓,2,   Warburg↓,2,   Zeb1↓,1,   ZO-1↑,1,  
Total Targets: 54

Results for Effect on Normal Cells:
antiOx↑,1,   BioAv↓,1,   Dose↝,1,   eff↑,1,   GPx↑,1,   GutMicro↑,1,   IL1β↓,1,   Inflam↓,1,   NRF2↑,1,   PGE2↓,1,   ROS↓,1,   TGF-β↑,1,   TNF-α↓,1,   Weight↓,1,   ZO-1↑,1,  
Total Targets: 15

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