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⟱

3454-

ALA,

Lipoic acid blocks autophagic flux and impairs cellular bioenergetics in breast cancer and reduces stemness

in-vitro,

BC,

MCF-7

(0.5 mM, 1 mM, 2.5 mM, and 5 mM)

in-vitro,

BC,

MDA-MB-231

TumCG↑, Lipoic acid inhibits breast cancer cell growth via accumulation of autophagosomes.
Glycolysis↓, Lipoic acid inhibits glycolysis in breast cancer cells.
ROS↑, Lipoic acid induces ROS production in breast cancer cells/BCSC.
CSCs↓, Here, we demonstrate that LA inhibits mammosphere formation and subpopulation of BCSCs
selectivity↑, In contrast, LA at similar doses. had no significant effect on the cell viability of the human embryonic kidney cell line (HEK-293)
LC3B-II↑, LA treatment (0.5 mM and 1.0 mM) increased the expression level of LC3B-I to LC3B-II in both MCF-7 and MDA-MB231cells at 48 h
MMP↓, LA induced mitochondrial ROS levels, decreased mitochondria complex I activity, and MMP in both MCF-7 and MDA-MB231 cells
mitResp↓, In MCF-7 cells, we found a substantial reduction in maximal respiration and ATP production at 0.5 mM and 1 mM of LA treatment after 48 h
ATP↓,
OCR↓, LA at 2.5 mM decreased OCR
NAD↓, we found that LA (0.5 mM and 1 mM) significantly reduced ATP production and NAD levels in MCF-7 and MDA-MB231 cells
p‑AMPK↑, LA treatment (0.5 mM and 1.0 mM) increased p-AMPK levels;
GlucoseCon↓, LA (0.5 mM and 1 mM) significantly decreased glucose uptake and lactate production in MCF-7, whereas LA at 1 mM significantly reduced glucose uptake and lactate production in MDA-MB231 cells but it had no effect at 0.5 mM
lactateProd↓,
HK2↓, LA reduced hexokinase 2 (HK2), phosphofructokinase (PFK), pyruvate kinase M2 (PKM2), and lactate dehydrogenase A (LDHA) expression in MCF-7 and MDA-MB231 cells
PFK↓,
LDHA↓,
eff↓, Moreover, we found that LA-mediated inhibition of cellular bioenergetics including OCR (maximal respiration and ATP production) and glycolysis were restored by NAC treatment (Fig. 6E and F) which indicates that LA-induced ROS production is responsibl
mTOR↓, LA inhibits mTOR signaling and thereby decreased the p-TFEB levels in breast cancer cells
ECAR↓, LA also inhibits glycolysis as evidenced by decreased glucose uptake, lactate production, and ECAR.
ALDH↓, LA decreased ALDH1 activity, CD44+/CD24-subpopulation, and increased accumulation of autophagosomes possibly due to inhibition of autophagic flux of breast cancer.
CD44↓,
CD24↓,

710-

Bor,

Boric acid inhibits stored Ca2+ release in DU-145 prostate cancer cells

in-vitro,

Pca,

DU145

NAD↓, inhibits NAD+ and NADP+
TumCP↓, Cell proliferation was inhibited by 30% at 100 microM, 60% at 250 microM, and 97% at 1,000 microM BA
CD38↑,
Ca+2↓, hypothesize that toxicity of BA stems from the ability of high concentrations to impair Ca2+ signaling.

4468-

VitC,

SSE,

Selenium modulates cancer cell response to pharmacologic ascorbate

in-vivo,

GBM,

U87MG

in-vitro,

CRC,

HCT116

eff↓, In vivo, dietary selenium deficiency resulted in significant enhancement of ascorbate activity against glioblastoma xenografts
TumCD↑, pharmacologic ascorbate raises the serum ascorbate concentration into the millimolar range, a concentration at which ascorbate has been shown to kill cancer cells in vitro
ChemoSen↑, Pharmacologic ascorbate has been shown to synergize with multiple chemotherapeutic agents in animal models and is well-tolerated in human patients [1,4], motivating ongoing clinical trials.
ROS⇅, Indeed, the role of ascorbate as either a pro- or anti-oxidant has been suggested to depend on concentration, with low doses mitigating ROS and high doses generating them
DNAdam↑, H2O2 generation by ascorbate has been associated with DNA damage and subsequent PARP activation, which can deplete NAD and thereby inhibit glycolysis
PARP↑,
NAD↓,
Glycolysis↓,
Fenton↑, Ascorbate cytotoxicity depends on the intracellular labile iron pool (Fig 1a) [3,9]. One explanation for this phenomenon is that ascorbate-generated H2O2 causes toxicity through Fenton chemistry
lipid-P↑, extensive lipid peroxidation
eff↓, More generally, they establish dietary selenium depletion as a potential means of sensitizing tumors to free radical stress.
H2O2↑, High concentrations (mM) of ascorbate have been shown to generate H2O2 in vitro
other↝, Selenium supplementation has been shown to protect cells against iron-dependent cell death by supporting increased expression of selenoproteins, including GPX4, which defend against oxidative stress

633-

VitC,

Diverse antitumor effects of ascorbic acid on cancer cells and the tumor microenvironment

Analysis,

NA,

Fenton↑,
ROS↑,
EMT↓, Ascorbic acid is also known to inhibit EMT of tumor cells
DNAdam↑,
PARP↑, DNA damage increases PARP activity, thereby decreasing NAD+ levels
NAD↓, NAD+
ATP↓,
Apoptosis↑,

630-

VitC,

Metabolomic alterations in human cancer cells by vitamin C-induced oxidative stress

in-vitro,

BC,

MCF-7

2.4 mM

in-vitro,

BC,

HT-29

TCA↑,
ATP↓,
NAD↓, vitamin C caused cell death through NAD depletion in MCF7 and HT29 cells
H2O2↑,
GSH/GSSG↓,

629-

VitC,

Cu,

Fe,

The antioxidant ascorbic acid mobilizes nuclear copper leading to a prooxidant breakage of cellular DNA: implications for chemotherapeutic action against cancer

in-vitro,

NA,

ROS↑,
DNAdam↑,
NAD↓,

628-

VitC,

Mg,

Enhanced Anticancer Effect of Adding Magnesium to Vitamin C Therapy: Inhibition of Hormetic Response by SVCT-2 Activation

in-vivo,

Colon,

CT26

mouse

in-vitro,

NA,

MCF-7

 1–10 mM(Mg)

(MgSO4 and MgCl2) no cytotoxicity at any of the tested concentrations.

in-vitro,

NA,

SkBr3

AntiCan↑, combined vit c and Mg
SVCT-2↝, Cancer cells that showed high SVCT-2 expression levels were more sensitive to AA treatment (SVCT-2 expression was not changed)
TumCD↑, MgSO4 and MgCl2 significantly increased the cell deaths caused by vitamin C treatment
ROS↑,
P21↑,
proCasp3↑,
TumVol↓, cotreating with vitamin C and magnesium ions inhibited tumor growth more effectively than treating with only vitamin C (mouse)
DNAdam↑,
NAD↓,

Showing Research Papers: 1 to 7 of 7

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 7

Pathway results for Effect on Cancer / Diseased Cells:

Functional Outcomes ⓘ

AntiCan↑, 1, TumVol↓, 1,
Total Targets: 44

Pathway results for Effect on Normal Cells:

Total Targets: 0

Scientific Paper Hit Count for: NAD, Nicotinamide adenine dinucleotide

5 Vitamin C (Ascorbic Acid)
1 Alpha-Lipoic-Acid
1 Boron
1 Selenite (Sodium)
1 Copper and Cu NanoParticles
1 Iron
1 Magnesium

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

Filter Conditions: Pro/AntiFlg:%  IllCat:%  CanType:%  Cells:%  prod#:%  Target#:815  State#:%  Dir#:1
  wNotes=on  sortOrder:rid,rpid

NAD Cancer Research Results

Pathway results for Effect on Cancer / Diseased Cells:

Redox & Oxidative Stress ⓘ

Mitochondria & Bioenergetics ⓘ

Core Metabolism/Glycolysis ⓘ

Cell Death ⓘ

Transcription & Epigenetics ⓘ

Autophagy & Lysosomes ⓘ

DNA Damage & Repair ⓘ

Cell Cycle & Senescence ⓘ

Proliferation, Differentiation & Cell State ⓘ

Migration ⓘ

Barriers & Transport ⓘ

Drug Metabolism & Resistance ⓘ

Functional Outcomes ⓘ

Pathway results for Effect on Normal Cells:

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