ADP:ATP Cancer Research Results

ADP:ATP, ADP/ATP ratio: Click to Expand ⟱
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ADP/ATP ratio is a key indicator of a cell’s energy state and mitochondrial function. In the context of cancer, shifts in the ADP/ATP ratio reflect changes in metabolic activity, mitochondrial efficiency, and overall cellular bioenergetics.
The ADP/ATP ratio reflects the balance between energy consumption and production. A high ADP/ATP ratio indicates lower energy reserves (or higher energy consumption), while a low ratio suggests abundant ATP availability.
• Mitochondrial Function and Metabolism:
– Cancer cells often reprogram their metabolism (the “Warburg effect”) to favor glycolysis even in the presence of oxygen. This metabolic shift can affect the ADP/ATP ratio.
– Mitochondrial dysfunction, commonly observed in tumors, may also lead to altered ADP/ATP ratios, impacting how cells respond to metabolic stress.

• Elevated ADP/ATP Ratio:
– In some aggressive tumors, an elevated ADP/ATP ratio can be a sign of mitochondrial stress or increased energy turnover.
– This state may result from rapid proliferation, increased energy demand, or inefficient ATP production.

• Reduced ADP/ATP Ratio:
– Alternatively, some cancer cells may maintain a lower ADP/ATP ratio by upregulating glycolysis or oxidative phosphorylation, ensuring a steady ATP supply to fuel growth and survival.
– Tumors with a robust bioenergetic capacity may display lower ratios, possibly correlating with resistance to energetic stress.

An elevated or imbalanced ADP/ATP ratio has been associated with aggressive tumor behavior and may predict poor prognosis in certain contexts, although its exact role can vary by tumor type.
Scientific Papers found: Click to Expand⟱
3391- ART/DHA,    Antitumor Activity of Artemisinin and Its Derivatives: From a Well-Known Antimalarial Agent to a Potential Anticancer Drug
- Review, Var, NA
TumCP↓, inhibiting cancer proliferation, metastasis, and angiogenesis.
TumMeta↓,
angioG↓,
TumVol↓, reduces tumor volume and progression
BioAv↓, artemisinin has low solubility in water or oil, poor bioavailability, and a short half-life in vivo (~2.5 h)
Half-Life↓,
BioAv↑, semisynthetic derivatives of artemisinin such as artesunate, arteeter, artemether, and artemisone have been effectively used as antimalarials with good clinical efficacy and tolerability
eff↑, preloading of cancer cells with iron or iron-saturated holotransferrin (diferric transferrin) triggers artemisinin cytotoxicity
eff↓, Similarly, treatment with desferroxamine (DFO), an iron chelator, renders compounds inactive
ROS↑, ROS generation may contribute with the selective action of artemisinin on cancer cells.
selectivity↑, Tumor cells have enhanced vulnerability to ROS damage as they exhibit lower expression of antioxidant enzymes such as superoxide dismutase, catalase, and gluthatione peroxidase compared to that of normal cells
TumCCA↑, G2/M, decreased survivin
survivin↓,
BAX↑, Increased Bax, activation of caspase 3,8,9 Decreased Bc12, Cdc25B, cyclin B1, NF-κB
Casp3↓,
Casp8↑,
Casp9↑,
CDC25↓,
CycB/CCNB1↓,
NF-kB↓,
cycD1/CCND1↓, decreased cyclin D, E, CDK2-4, E2F1 Increased Cip 1/p21, Kip 1/p27
cycE/CCNE↓,
E2Fs↓,
P21↑,
p27↑,
ADP:ATP↑, Increased poly ADP-ribose polymerase Decreased MDM2
MDM2↓,
VEGF↓, Decreased VEGF
IL8↓, Decreased NF-κB DNA binding [74, 76] IL-8, COX2, MMP9
COX2↓,
MMP9↓,
ER Stress↓, ER stress, degradation of c-MYC
cMyc↓,
GRP78/BiP↑, Increased GRP78
DNAdam↑, DNA damage
AP-1↓, Decreased NF-κB, AP-1, Decreased activation of MMP2, MMP9, Decreased PKC α/Raf/ERK and JNK
MMP2↓,
PKCδ↓,
Raf↓,
ERK↓,
JNK↓,
PCNA↓, G2, decreased PCNA, cyclin B1, D1, E1 [82] CDK2-4, E2F1, DNA-PK, DNA-topo1, JNK VEGF
CDK2↓,
CDK4↓,
TOP2↓, Inhibition of topoisomerase II a
uPA↓, Decreased MMP2, transactivation of AP-1 [56, 88] NF-κB uPA promoter [88] MMP7
MMP7↓,
TIMP2↑, Increased TIMP2, Cdc42, E cadherin
Cdc42↑,
E-cadherin↑,

2790- CHr,    Chrysin: Pharmacological and therapeutic properties
- Review, Var, NA
*hepatoP↑, graphical abstract
*neuroP↓,
*ROS↓,
*cardioP↑,
*Inflam↓,
eff↑, suppression of hTERT and cyclin D1 gene expression in T47D breast cancer cell lines is due to the combined effect of metformin and chrysin
hTERT/TERT↓,
cycD1/CCND1↓,
MMP9↓, nanoparticle-based chrysin in C57B16 mice bearing B16F10 melanoma tumors was markedly presented reductions in the levels of MMP-9, MMP-2, and TERT genes, whereas it enhanced TIMP-2 andTIMP-1 genes expression
MMP2↓,
TIMP1↑,
TIMP2↑,
BioAv↑, nano-encapsulation of chrysin and curcumin improved the delivery of these phytochemicals that significantly inhibited the growth of cancer cells, while it decreased the hTERT gene expression via increased solubility and bioavailability
HK2↓, chrysin treatment restrained tumor growth in HCC xenograft models and significantly reduced HK-2 expression in tumor tissue
ROS↑, showing a significant increase in intracellular reactive oxygen species (ROS), cytotoxicity, mitochondrial membrane potential (MMP) collapse, caspase-3 activation, ADP/ATP ratio, and ultimately apoptosis
MMP↓,
Casp3↑,
ADP:ATP↑,
Apoptosis↑,
ER Stress↑, Likewise, chrysin encouraged endoplasmic reticulum (ER) stress via stimulation of unfolded protein response (UPR
UPR↑,
GRP78/BiP↝, (eIF2α), PRKR-like ER kinase (PERK) and 78 kDa glucose-regulated protein (GRP78).
eff↑, silibinin and chrysin synergistically inhibited growth of T47D BCC and downregulated the hTERT and cyclin D1 level
Ca+2↑, Primarily, increased ROS and cytoplasmic Ca 2+ levels alongside induction of cell death and loss of MMP are involved in inhibition of ovarian cancer through chrysin.

1249- CHr,    Chrysin as an Anti-Cancer Agent Exerts Selective Toxicity by Directly Inhibiting Mitochondrial Complex II and V in CLL B-lymphocytes
- in-vitro, CLL, NA
ROS↑,
MMP↓,
ADP:ATP↑,
Casp3↑,
Apoptosis↑,


Showing Research Papers: 1 to 3 of 3

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 3

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

ROS↑, 3,  

Mitochondria & Bioenergetics ⓘ

ADP:ATP↑, 3,   CDC25↓, 1,   MMP↓, 2,   Raf↓, 1,  

Core Metabolism/Glycolysis ⓘ

cMyc↓, 1,   HK2↓, 1,  

Cell Death ⓘ

Apoptosis↑, 2,   BAX↑, 1,   Casp3↓, 1,   Casp3↑, 2,   Casp8↑, 1,   Casp9↑, 1,   hTERT/TERT↓, 1,   JNK↓, 1,   MDM2↓, 1,   p27↑, 1,   survivin↓, 1,  

Protein Folding & ER Stress ⓘ

ER Stress↓, 1,   ER Stress↑, 1,   GRP78/BiP↑, 1,   GRP78/BiP↝, 1,   UPR↑, 1,  

DNA Damage & Repair ⓘ

DNAdam↑, 1,   PCNA↓, 1,  

Cell Cycle & Senescence ⓘ

CDK2↓, 1,   CDK4↓, 1,   CycB/CCNB1↓, 1,   cycD1/CCND1↓, 2,   cycE/CCNE↓, 1,   E2Fs↓, 1,   P21↑, 1,   TumCCA↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

ERK↓, 1,   TOP2↓, 1,  

Migration ⓘ

AP-1↓, 1,   Ca+2↑, 1,   Cdc42↑, 1,   E-cadherin↑, 1,   MMP2↓, 2,   MMP7↓, 1,   MMP9↓, 2,   PKCδ↓, 1,   TIMP1↑, 1,   TIMP2↑, 2,   TumCP↓, 1,   TumMeta↓, 1,   uPA↓, 1,  

Angiogenesis & Vasculature ⓘ

angioG↓, 1,   VEGF↓, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 1,   IL8↓, 1,   NF-kB↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 1,   BioAv↑, 2,   eff↓, 1,   eff↑, 3,   Half-Life↓, 1,   selectivity↑, 1,  

Clinical Biomarkers ⓘ

hTERT/TERT↓, 1,  

Functional Outcomes ⓘ

TumVol↓, 1,  
Total Targets: 61

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

ROS↓, 1,  

Immune & Inflammatory Signaling ⓘ

Inflam↓, 1,  

Functional Outcomes ⓘ

cardioP↑, 1,   hepatoP↑, 1,   neuroP↓, 1,  
Total Targets: 5

Scientific Paper Hit Count for: ADP:ATP, ADP/ATP ratio
2 Chrysin
1 Artemisinin
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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