nicotinamide adenine dinucleotide / cGAS–STING Cancer Research Results

NAD, nicotinamide adenine dinucleotide: Click to Expand ⟱
Features:
(Nicotinamide adenine dinucleotide) is a vital coenzyme found in all living cells.
• It exists in two forms: oxidized (NAD⁺) and reduced (NADH), playing central roles in redox reactions, energy metabolism, and various signaling pathways.
• NAD⁺ is essential for critical cellular processes, including ATP production, DNA repair (via enzymes like PARPs), and regulation of sirtuins (a family of NAD⁺-dependent deacetylases involved in cellular stress responses and longevity).

NAD⁺ is integral to energy metabolism, redox balance, DNA repair, and cellular regulatory functions—processes that are often dysregulated in cancer.
-It is required for over 500 enzymatic reactions and plays key roles in the regulation of almost all major biological processes

Medicor Cancer Centres offers it:

-involved in glycolysis, the tricarboxylic acid (TCA) cycle, and oxidative phosphorylation.
-NMN is a precursor to nicotinamide adenine dinucleotide (NAD+)
-alternative form of vitamin B, amide of nicotinic acid
-NAD+ levels decline as we age
-high dose NMN promotes ferroptosis through NAM-mediated SIRT1-AMPK-ACC signaling
-At low doses (10 and 20 mM) and prolonged exposure (48 h), NMN increased cell proliferation, but it induced the suppression of cell proliferation at the high dose (100 mM)
-VitB3 and niacin are precursors for the synthesis of NAD in the body

NAD in Cancer Is Dual-Edge
Tumors need NAD+ to sustain:
-Glycolysis (Warburg)
-PARP DNA repair
-Sirtuin survival signaling
-Redox buffering
NAD depletion (via NAMPT inhibition or high PARP consumption) can:
-Collapse ATP
-Increase ROS
-Trigger apoptosis

Rank Pathway / Axis Cancer / Tumor Context Normal Tissue Context TSF Primary Effect Notes / Interpretation
1 NAD+ salvage pathway (NAMPT → NMN → NAD+) NAD+ pool ↑ supports glycolysis, DNA repair, PARP activity; NAMPT often upregulated Maintains metabolic homeostasis R, G Metabolic support node Many tumors depend on NAMPT-driven NAD+ salvage; NAMPT inhibitors (e.g., FK866) deplete NAD+ and induce energetic collapse.
2 Glycolysis support (LDH-dependent NAD+ recycling) NAD+ regeneration sustains Warburg flux Normal glycolytic tissues also require NAD+ P, R Warburg sustainment LDH converts NADH → NAD+ to maintain glycolytic flux; NAD+ availability is a rate-limiting factor in high glycolysis tumors.
3 PARP-mediated DNA repair (NAD+ consumption) DNA damage repair ↑; therapy resistance ↑ (context) Genome stability maintenance R, G DNA repair capacity PARPs consume NAD+ during DNA repair. PARP inhibitors exploit tumors with HR defects (e.g., BRCA).
4 Sirtuin signaling (SIRT1–7; NAD+-dependent deacetylases) Context-dependent tumor survival or suppression Metabolic regulation, longevity pathways R, G Epigenetic/metabolic modulation Sirtuins require NAD+; effects vary by tumor type (pro-survival in some, suppressive in others).
5 Redox balance (NAD+/NADH ratio) High NAD+/NADH ratio supports anabolic growth Redox homeostasis P, R Redox control Altered NAD+/NADH ratios influence ROS, mitochondrial function, and metabolic flexibility.
6 CD38/CD157 NAD+ degradation NAD+ depletion influences immune and tumor metabolism Immune modulation, aging R, G Immune-metabolic interface CD38 overexpression can lower NAD+ pools; relevant in immune microenvironment contexts.
7 OXPHOS support (mitochondrial NADH supply) NADH fuels ETC; supports mitochondrial ATP production Normal energy metabolism P, R Mitochondrial respiration support NADH oxidation via Complex I regenerates NAD+; OXPHOS-dependent tumors rely on this axis.
8 Therapy resistance modulation NAD+ restoration may reduce oxidative therapy efficacy May protect normal tissue from oxidative injury G Context-dependent NAD+ boosting (e.g., NR, NMN) may theoretically support tumor repair pathways; data mixed and context-specific.
9 NAMPT inhibition (therapeutic strategy) NAD+ depletion → ATP ↓ → apoptosis ↑ Toxicity risk in high-turnover tissues R, G Metabolic collapse NAMPT inhibitors are being explored as anti-cancer metabolic therapies.
10 Bioavailability / supplementation constraint Systemic NAD+ boosting may not selectively target tumor NAD pools Systemic NAD+ supports normal tissue repair — Translation constraint Oral precursors (NR, NMN, niacin) increase systemic NAD+ but tumor-specific impact remains unclear.

TSF: P = 0–30 min (redox flux shifts), R = 30 min–3 hr (metabolic signaling changes), G = >3 hr (gene-level adaptation, repair, phenotype changes).



cGAS–STING, GMP-AMP synthase (cGAS) and stimulator of interferon genes (STING): Click to Expand ⟱
Source:
Type:
cGAS–STING pathway is primarily associated with neuroinflammation and neuronal damage.
-Studies show upregulated STING in microglia and astrocytes in AD models.
Scientific Papers found: Click to Expand⟱
4035- NAD,  VitB3,    NAD+ supplementation reduces neuroinflammation and cell senescence in a transgenic mouse model of Alzheimer's disease via cGAS-STING
- in-vitro, AD, NA
*Inflam↓, *DNAdam↓, *NLRP3↓, *cGAS–STING↓,

Showing Research Papers: 1 to 1 of 1

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 1

Pathway results for Effect on Cancer / Diseased Cells:


Total Targets: 0

Pathway results for Effect on Normal Cells:


DNA Damage & Repair ⓘ

DNAdam↓, 1,  

Immune & Inflammatory Signaling ⓘ

Inflam↓, 1,  

Cellular Microenvironment ⓘ

cGAS–STING↓, 1,  

Protein Aggregation ⓘ

NLRP3↓, 1,  
Total Targets: 4

Scientific Paper Hit Count for: cGAS–STING, GMP-AMP synthase (cGAS) and stimulator of interferon genes (STING)
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#:268  Target#:1370  State#:%  Dir#:%
  wNotes=0  sortOrder:rid,rpid

 

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