NAD Cancer Research Results

NAD, Nicotinamide adenine dinucleotide: Click to Expand ⟱
Source:
Type: coenzyme
NAD generally refers to the oxidized form, known as NAD⁺
NAD (Nicotinamide adenine dinucleotide) is a coenzyme that plays a crucial role in various cellular processes, including energy metabolism, DNA repair, and cell signaling. Research has shown that NAD levels are often decreased in cancer cells, and this decrease can contribute to the development and progression of cancer.
NAD is a coenzyme that plays a central role in energy metabolism, DNA repair, and cell signaling. It exists in two forms: NAD+ (oxidized) and NADH (reduced).

NADH is the reduced form of NAD⁺. When NAD⁺ accepts electrons (typically during metabolic processes like glycolysis, the citric acid cycle, and beta-oxidation), it becomes NADH.

NADPH, on the other hand, is a phosphorylated form of NADP+, which is a related coenzyme. NADPH is primarily involved in anabolic reactions, such as fatty acid synthesis, cholesterol synthesis, and antioxidant defenses.
Scientific Papers found: Click to Expand⟱
1869- DCA,    Dichloroacetate induces autophagy in colorectal cancer cells and tumours
- in-vitro, CRC, HT-29 - in-vitro, CRC, HCT116 - in-vitro, Pca, PC3 - in-vitro, CRC, HT-29
LC3II↑, Increased expression of the autophagy markers LC3B II was observed following DCA treatment both in vitro and in vivo
ROS↑, increased production of reactive oxygen species (ROS)
mTOR↓, mTOR inhibition
MCT1↓, DCA is a possible competitive MCT-1 inhibitor
NADH:NAD↓, increased NAD+/NADH ratios
NAD↑,
TumAuto↑, DCA induces autophagy in cancer cells accompanied by ROS production and mTOR inhibition, reduced lactate excretion, reduced kPL and increased NAD+/NADH ratio.
lactateProd↓, DCA treatment reduces lactate excretion with no change in glucose uptake
LDH↑, Increased LDH activity

2247- MF,    Effects of Pulsed Electromagnetic Field Treatment on Skeletal Muscle Tissue Recovery in a Rat Model of Collagenase-Induced Tendinopathy: Results from a Proteome Analysis
- in-vivo, Nor, NA
*Glycolysis↓, PEMF-treated animals exhibited decreased glycolysis and increased LDHB expression, enhancing NAD signaling and ATP production
*LDHB↑,
*NAD↑,
*ATP↑,
*antiOx↑, Antioxidant protein levels increased, controlling ROS production.
*ROS↑,
*YAP/TEAD↑, upregulation of YAP and PGC1alpha and increasing slow myosin isoforms, thus speeding up physiological recovery.
*PGC-1α↑,
*TCA↑, increased in PEMF-treated injured limbs
*FAO↑,
*OXPHOS↑, Oxidative phosphorylation was increased in the muscle of injured rats that underwent PEMF treatment

2963- PL,    Piperlongumine activates Sirtuin1 and improves cognitive function in a murine model of Alzheimer’s disease
- in-vitro, AD, HEK293
*SIRT1↑, Piperlongumine (PL) activates the deacetylase ability of Sirt1 in vitro.
*cognitive↑, PL improves cognitive deficits in APP/PS1 mice.
*Aβ↓, PL reduces amyloid deposition and neuro-inflammation in the brain of APP/PS1 mice.
*Inflam↓,
*neuroP↑,
memory↑, Sirt1 has been shown to modulate synaptic plasticity and memory formation
Dose↓, PL induced Sirt1 deacetylase activity at a relatively low concentration, i.e. 1.5 uM, compared to the resveratrol treatment.
NAD↑, PL treatment at doses of 0.5 and 4 μM significantly increased the level of NAD + . These results indicate that PL might activate Sirt1, subsequently changing the NAD + /NADH ratio

4703- PTS,  RES,    Pterostilbene and resveratrol: Exploring their protective mechanisms against skin photoaging - A scoping review
- NA, Nor, NA
*AntiAge↑, resveratrol shows significant promise in combating skin photoaging, pterostilbene is still in the early exploration phases.
*eff↑, Pterostilbene demonstrates potential to outperform resveratrol
*Inflam↓, well known for properties, such as anti-aging, anti-inflammatory, anti-melanogenesis, and anti-cancer
*AntiCan↑,
*ROS↓, Pterostilbene significantly prevented UVB-induced reduction in cell viability and increased reactive oxygen species (ROS) production
*Catalase↑, pterostilbene significantly increased gene expression of catalase (CAT)
*GSR↑, glutathione reductase (GSR), heme oxygenase-1 (HMOX-1) and NAD(P)H quinone dehydrogenase 1 (NQO1);
*HO-1↑,
*NAD↑,
*NQO1↑,
*SOD↑, while significantly increasing glutathione disulfide (GSSH), SOD, nuclear Nrf2,
*NRF2↑,

2553- SFN,    Mechanistic review of sulforaphane as a chemoprotective agent in bladder cancer
- Review, Bladder, NA
antiOx↓, SFN is a bioactive compound with both antioxidant and anti-inflammatory properties.
Inflam↓,
ChemoSen↑, SFN also improves the efficacy of certain traditional chemotherapeutic regimens
ROS⇅, A lesser established mechanism proposed by Li, et al. is that SFN induces mild increases ROS, leading to transcription factor EB (TFEB) activation. TFEB plays a role in activating antioxidant response elements and...ultimately reducing overall oxidat
*NRF2↑, SFN treatment increased Nrf2 and, therefore, glutathione levels
*GSH↑,
Catalase↑, Cancer cells treated with SFN showed higher catalase levels, heme oxygenase 1, and NAD(P)
HO-1↑,
NAD↑,
chemoP↑, Taken together, these studies provide strong evidence for the chemoprotective nature of SFN in various human epithelial cancers, including those of the bladder.

3330- SIL,    Mechanistic Insights into the Pharmacological Significance of Silymarin
- Review, Var, NA
*neuroP↑, silymarin is employed significantly as a neuroprotective, hepatoprotective, cardioprotective, antioxidant, anti-cancer, anti-diabetic, anti-viral, anti-hypertensive, immunomodulator, anti-inflammatory, photoprotective and detoxification agent
*hepatoP↑,
*cardioP↑,
*antiOx↓,
*NLRP3↓, Zhang et al. (2018) observed that silybin significantly impedes NLR family pyrin domain containing 3 (NLRP3) inflammasome activation in NAFLD by elevating NAD+ levels,
*NAD↑,
ROS↓, MDA-MB-231: it was observed that silybin treatment also abolishes activation of the NLRP3 inflammasome through repression of ROS generation, resulting in reduced tumor cell migration and invasion
NLRP3↓,
TumCMig↓,
*COX2↓, mpairing several enzymes (COX-2, iNOS, SGPT, SGOT, MMP, MPO, AChE, G6Pase, MAO-B, LDH, Telomerase, FAS and CK-MB)
*iNOS↓,
*MPO↓,
*AChE↓,
*LDH↓,
*Telomerase↓,
*Fas↓,

3422- TQ,    Thymoquinone, as a Novel Therapeutic Candidate of Cancers
- Review, Var, NA
selectivity↑, TQ selectively inhibits the cancer cells’ proliferation in leukemia [9], breast [10], lungs [11], larynx [12], colon [13,14], and osteosarcoma [15]. However, there is no effect against healthy cells
P53↑, It also re-expressed tumor suppressor genes (TSG), such as p53 and Phosphatase and tensin homolog (PTEN) in lung cancer
PTEN↑,
NF-kB↓, antitumor properties by regulating different targets, such as nuclear factor kappa B (NF-Kb), peroxisome proliferator-activated receptor-γ (PPARγ), and c-Myc [1], which resulted in caspases protein activation
PPARγ↓,
cMyc↓,
Casp↑,
*BioAv↓, Due to hydrophobicity, there are limitations in the bioavailability and drug formation of TQ.
BioAv↝, TQ is sensitive to light; a short period of exposure results in severe degradation, regardless of the solution’s acidity and solvent type [27]. It is also unstable in alkaline solutions because TQ’s stability decreases with rising pH
eff↑, Encapsulating TQ with CS improves the uptake and bioavailability of TQ but has low encapsulation efficiency (35%)
survivin↓, TQ showed antiproliferative and pro-apoptotic potency on breast cancer through the suppression of anti-apoptotic proteins, such as survivin, Bcl-xL, and Bcl-2
Bcl-xL↓,
Bcl-2↓,
Akt↓, treating doxorubicin-resistant MCF-7/DOX cells with TQ inhibited Akt and Bcl2 phosphorylation and increased the expression of PTEN and apoptotic regulators such as Bax, cleaved PARP, cleaved caspases, p53, and p21 [
BAX↑,
cl‑PARP↑,
CXCR4↓, inhibited metastasis with significant inhibition of chemokine receptor Type 4 (CXCR4), which is considered a poor prognosis indicator, matrix metallopeptidase 9 (MMP9), vascular endothelial growth factor Receptor 2 (VEGFR2), Ki67, and COX2
MMP9↓,
VEGFR2↓,
Ki-67↓,
COX2↓,
JAK2↓, TQ at 25, 50 and 75 µM inhibited JAK2 and c-Src activity and induced apoptosis by inhibiting the phosphorylation of STAT3 and STAT3 downstream genes, such as Bcl-2, cyclin D, survivin, and VEGF, and upregulating caspases-3, caspases-7, and caspases-9
cSrc↓,
Apoptosis↑,
p‑STAT3↓,
cycD1/CCND1↓,
Casp3↑,
Casp7↑,
Casp9↑,
N-cadherin↓, downregulated the mesenchymal genes expression N-cadherin, vimentin, and TWIST, while upregulating epithelial genes like E-cadherin and cytokeratin-19.
Vim↓,
Twist↓,
E-cadherin↑,
ChemoSen↑, The combined treatment of 5 μM TQ and 2 μg/mL cisplatin was more effective in cancer growth and progression than either agent alone in a xenograft tumor mouse model.
eff↑, TQ–artemisinin hybrid therapy (2.6 μM) showed an enhanced ROS generation level and concomitant DNA damage induction in human colon cancer cells, while not affecting nonmalignant colon epithelial at 100 μM
EMT↓, TQ inhibits the survival signaling pathways to reduce carcinogenesis progress rate, and decreases cancer metastasis through regulation of epithelial to mesenchymal transition (EMT).
ROS↑, Apoptosis is induced by TQ in cancer cells through producing ROS, demethylating and re-expressing the TSG
DNMT1↓, inhibits DNMT1, figure 2
eff↑, TQ–vitamin D3 combination significantly reduced pro-cancerous molecules (Wnt, β-catenin, NF-κB, COX-2, iNOS, VEGF and HSP-90) a
EZH2↓, reduced angiogenesis by downregulating significant angiogenic genes such as versican (VCAN), the growth factor receptor-binding protein 2 (Grb2), and enhancer of zeste homolog 2 (EZH2), which participates in histone methylatio
hepatoP↑, Moreover, TQ improved liver function as well as reduced hepatocellular carcinoma progression
Zeb1↓, TQ decreases the Twist1 and Zeb1 promoter activities,
RadioS↑, TQ combined with radiation inhibited proliferation and induced apoptosis more than a TQ–cisplatin combination against SCC25 and CAL27 cell lines
HDAC↓, TQ has inhibited the histone deacetylase (HDAC) enzyme and reduced its total activity.
HDAC1↓, as well as decreasing the expression of HDAC1, HDAC2, and HDAC3 by 40–60%
HDAC2↓,
HDAC3↓,
*NAD↑, In non-cancer cells, TQ can increase cellular NAD+
*SIRT1↑, An increase in the levels of intracellular NAD+ led to the activation of the SIRT1-dependent metabolic pathways
SIRT1↓, On the other hand, TQ induced apoptosis by downregulating SIRT1 and upregulating p73 in the T cell leukemia Jurkat cell line
*Inflam↓, TQ treatment of male Sprague–Dawley rats has reduced the inflammatory markers (CRP, TNF-α, IL-6, and IL-1β) and anti-inflammatory cytokines (IL-10 and IL-4) triggered by sodium nitrite
*CRP↓,
*TNF-α↓,
*IL6↓,
*IL1β↓,
*eff↑, The TQ–piperin combination has also decreased the oxidative damage triggered by microcystin in liver tissue and reduced malondialdehyde (MDA) and NO, while inducing glutathione (GSH) levels and superoxide dismutase (SOD), catalase (CAT), and glutathi
*MDA↓,
*NO↓,
*GSH↑,
*SOD↑,
*Catalase↑,
*GPx↑,
PI3K↓, repressing the activation of vital pathways, such as JAK/STAT and PI3K/AKT/mTOR.
mTOR↓,

4316- VitB3,    Unraveling the molecular mechanisms of vitamin deficiency in Alzheimer's disease pathophysiology
- Review, AD, NA
*NAD↑, Vitamin B3 is a precursor for metabolic reactions, converting into NAD and NADP, essential for energy metabolism, DNA repair, and cellular signaling
*Aβ↓, Low levels of NAD slow metabolism, which delays Aβ clearance and contributes to plaque formation, a key feature of AD
*p‑tau↓, So, vitamin B3 is important for NAD synthesis, and its deficiency disrupts key pathways, promoting tau phosphorylation and Aβ accumulation

4034- VitB3,    Nicotinamide riboside restores cognition through an upregulation of proliferator-activated receptor-γ coactivator 1α regulated β-secretase 1 degradation and mitochondrial gene expression in Alzheimer’s mouse models
- in-vivo, AD, NA
*cognitive↑, dietary treatment of Tg2576 mice with 250 mg/kg/day of NR for 3 months significantly attenuates cognitive deterioration in Tg2576 mice and coincides with an increase in the steady-state levels of NAD+ in the cerebral cortex;
*NAD↑, Evidence shows that NR treatment increases intracellular NAD+ concentration and improves NAD+-dependent activities in the cell
*BACE↓, BACE1 protein content is decreased by NR treatment in primary neuronal cultures derived from Tg2576 embryos
*Aβ↓, thus preventing Aβ production in the brain.
*PGC-1α↑, NR might reduce the Aβ burden in AD brain via enhancing PGC-1α expression, which increases BACE1 ubiquitination, degradation, and improves mitochondrial metabolism

4031- VitB3,    Nicotinamide Riboside-The Current State of Research and Therapeutic Uses
- Review, NA, NA
*cardioP↑, Accumulating evidence on NRs’ health benefits has validated its efficiency across numerous animal and human studies for the treatment of a number of cardiovascular, neurodegenerative, and metabolic disorders.
*neuroP↑,
*NAD↑, Oral supplementation with NR has been shown to increase NAD+ levels in multiple tissues, along with increased SIRT activity [10,11], improved mitochondrial function [37], and regenerative potential of stem cells
*SIRT1↑,
*NADPH↑, Furthermore, NR is one of the NAD+ intermediates that also serves as a precursor of NADH, as well as hepatic NADP+ and NADPH
*ROS↓, Moreover, SIRT1 inhibits effects of oxidative stress in T2D mice
*IL2↓, NR can similarly decrease IL-2, IL-5, IL-6, and TNFα
*IL5↓,
*IL6↓,
*TNF-α↓,
*Inflam↓, Targeting IL-6 has been recently proposed as a promising treatment to block the inflammatory storm
*BioAv↝, the apparent oral bioavailability of a 1000 mg dose of NR was highly variable among individuals
*BioAv↑, NR was able to increase NAD+ levels in the liver of mice, exhibiting greater oral bioavailability than NAM, which was, in turn, more orally bioavailable than NA


Showing Research Papers: 1 to 10 of 10

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 10

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

antiOx↓, 1,   Catalase↑, 1,   HO-1↑, 1,   ROS↓, 1,   ROS↑, 2,   ROS⇅, 1,  

Core Metabolism/Glycolysis ⓘ

cMyc↓, 1,   lactateProd↓, 1,   LDH↑, 1,   NAD↑, 3,   NADH:NAD↓, 1,   PPARγ↓, 1,   SIRT1↓, 1,  

Cell Death ⓘ

Akt↓, 1,   Apoptosis↑, 1,   BAX↑, 1,   Bcl-2↓, 1,   Bcl-xL↓, 1,   Casp↑, 1,   Casp3↑, 1,   Casp7↑, 1,   Casp9↑, 1,   MCT1↓, 1,   survivin↓, 1,  

Kinase & Signal Transduction ⓘ

cSrc↓, 1,  

Transcription & Epigenetics ⓘ

EZH2↓, 1,  

Autophagy & Lysosomes ⓘ

LC3II↑, 1,   TumAuto↑, 1,  

DNA Damage & Repair ⓘ

DNMT1↓, 1,   P53↑, 1,   cl‑PARP↑, 1,  

Cell Cycle & Senescence ⓘ

cycD1/CCND1↓, 1,  

Proliferation, Differentiation & Cell State ⓘ

EMT↓, 1,   HDAC↓, 1,   HDAC1↓, 1,   HDAC2↓, 1,   HDAC3↓, 1,   mTOR↓, 2,   PI3K↓, 1,   PTEN↑, 1,   p‑STAT3↓, 1,  

Migration ⓘ

E-cadherin↑, 1,   Ki-67↓, 1,   MMP9↓, 1,   N-cadherin↓, 1,   TumCMig↓, 1,   Twist↓, 1,   Vim↓, 1,   Zeb1↓, 1,  

Angiogenesis & Vasculature ⓘ

VEGFR2↓, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 1,   CXCR4↓, 1,   Inflam↓, 1,   JAK2↓, 1,   NF-kB↓, 1,  

Protein Aggregation ⓘ

NLRP3↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↝, 1,   ChemoSen↑, 2,   Dose↓, 1,   eff↑, 3,   RadioS↑, 1,   selectivity↑, 1,  

Clinical Biomarkers ⓘ

EZH2↓, 1,   Ki-67↓, 1,   LDH↑, 1,  

Functional Outcomes ⓘ

chemoP↑, 1,   hepatoP↑, 1,   memory↑, 1,  
Total Targets: 68

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↓, 1,   antiOx↑, 1,   Catalase↑, 2,   GPx↑, 1,   GSH↑, 2,   GSR↑, 1,   HO-1↑, 1,   MDA↓, 1,   MPO↓, 1,   NQO1↑, 1,   NRF2↑, 2,   OXPHOS↑, 1,   ROS↓, 2,   ROS↑, 1,   SOD↑, 2,  

Mitochondria & Bioenergetics ⓘ

ATP↑, 1,   PGC-1α↑, 2,  

Core Metabolism/Glycolysis ⓘ

FAO↑, 1,   Glycolysis↓, 1,   LDH↓, 1,   LDHB↑, 1,   NAD↑, 7,   NADPH↑, 1,   SIRT1↑, 3,   TCA↑, 1,  

Cell Death ⓘ

Fas↓, 1,   iNOS↓, 1,   Telomerase↓, 1,   YAP/TEAD↑, 1,  

Angiogenesis & Vasculature ⓘ

NO↓, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 1,   CRP↓, 1,   IL1β↓, 1,   IL2↓, 1,   IL5↓, 1,   IL6↓, 2,   Inflam↓, 4,   TNF-α↓, 2,  

Synaptic & Neurotransmission ⓘ

AChE↓, 1,   p‑tau↓, 1,  

Protein Aggregation ⓘ

Aβ↓, 3,   BACE↓, 1,   NLRP3↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 1,   BioAv↑, 1,   BioAv↝, 1,   eff↑, 2,  

Clinical Biomarkers ⓘ

CRP↓, 1,   IL6↓, 2,   LDH↓, 1,  

Functional Outcomes ⓘ

AntiAge↑, 1,   AntiCan↑, 1,   cardioP↑, 2,   cognitive↑, 2,   hepatoP↑, 1,   neuroP↑, 3,  
Total Targets: 56

Scientific Paper Hit Count for: NAD, Nicotinamide adenine dinucleotide
3 Vitamin B3,Niacin
1 Dichloroacetate
1 Magnetic Fields
1 Piperlongumine
1 Pterostilbene
1 Resveratrol
1 Sulforaphane (mainly Broccoli)
1 Silymarin (Milk Thistle) silibinin
1 Thymoquinone
Query results interpretion may depend on "conditions" listed in the research papers.
Such Conditions may include : 
  -low or high Dose
  -format for product, such as nano of lipid formations
  -different cell line effects
  -synergies with other products 
  -if effect was for normal or cancerous cells

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