NADPH Cancer Research Results

NADPH, Nicotinamide adenine dinucleotide phosphate: Click to Expand ⟱
Source:
Type:
NADPH (Nicotinamide adenine dinucleotide phosphate) is a crucial molecule in cellular metabolism, playing a key role in various biological processes, including energy production, antioxidant defenses, and biosynthesis.
NADPH is essential for the proper functioning of the pentose phosphate pathway, which generates NADPH and ribose-5-phosphate. Cancer cells may exploit this pathway to support their high energy demands.
Many types of cancer, including breast, lung, and colon cancer, exhibit increased NADPH levels compared to normal tissues. This increase is often associated with enhanced glucose-6-phosphate dehydrogenase (G6PD) activity, a key enzyme in the pentose phosphate pathway that generates NADPH.
Pca, Prostate Cancer: Click to Expand ⟱
Prostate Cancer: Alterations in genes such as ERG, SPOP, MYC, androgen receptor (AR), and CHD1, drive PCa progression.
TP53 is the most commonly mutated gene in human cancer.
HH↑, GLI-1↑, SHH↑ P53↓
The loss of p53 and/or other tumor suppressor genes, reduced capacity for DNA repair, the dysfunction of telomerase activity, and changes in the pathways that govern the growth of cells also mediate the progression of Pca.
It has been well documented that Ca2+ influx and MDR1 upregulation are highly associated with GEM metabolism in human pancreatic carcinoma.
Increased Growth factor IGF-1/IGF-1R axis activation mediated by both PI3K/Akt or RAF/MEK/ERK system and AR expression remains important in the development and progression of prostate cancer.
It has been demonstrated that prostate cancer cells are relatively sensitive to heat stress.
Long non-coding RNA MALAT1 has been reported as an oncogenic target in multiple types of cancers, including PC.
Scientific Papers found: Click to Expand⟱
1985- PTL,    KEAP1 Is a Redox Sensitive Target That Arbitrates the Opposing Radiosensitive Effects of Parthenolide in Normal and Cancer Cells
- in-vitro, Pca, LNCaP - in-vitro, Pca, DU145 - in-vitro, Nor, PrEC - in-vivo, NA, NA
ROS↑, NADPH↑, RadioS↑, radioP↑, Trx↓, *ox-Keap1↑, ox-Keap1↓, rd-Keap1↑, *NRF2↑, NRF2∅, NF-kB↓,
1987- PTL,  Rad,    A NADPH oxidase dependent redox signaling pathway mediates the selective radiosensitization effect of parthenolide in prostate cancer cells
- in-vitro, Pca, PC3 - in-vitro, Nor, PrEC
selectivity↑, RadioS↑, ROS↑, *ROS∅, NADPH↑, Trx↓, PI3K↑, Akt↑, p‑FOXO3↓, SOD2↓, Catalase↓, radioP↑, *NADPH∅, *GSH↑, *GSH/GSSG↑, *NRF2↑,

Showing Research Papers: 1 to 2 of 2

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 2

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

Catalase↓, 1,   ox-Keap1↓, 1,   rd-Keap1↑, 1,   NRF2∅, 1,   ROS↑, 2,   SOD2↓, 1,   Trx↓, 2,  

Core Metabolism/Glycolysis ⓘ

NADPH↑, 2,  

Cell Death ⓘ

Akt↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

p‑FOXO3↓, 1,   PI3K↑, 1,  

Immune & Inflammatory Signaling ⓘ

NF-kB↓, 1,  

Drug Metabolism & Resistance ⓘ

RadioS↑, 2,   selectivity↑, 1,  

Functional Outcomes ⓘ

radioP↑, 2,  
Total Targets: 15

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

GSH↑, 1,   GSH/GSSG↑, 1,   ox-Keap1↑, 1,   NRF2↑, 2,   ROS∅, 1,  

Core Metabolism/Glycolysis ⓘ

NADPH∅, 1,  
Total Targets: 6

Scientific Paper Hit Count for: NADPH, Nicotinamide adenine dinucleotide phosphate
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:22  Cells:%  prod#:%  Target#:624  State#:%  Dir#:2
  wNotes=0  sortOrder:rid,rpid

 

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