ATP Cancer Research Results

ATP, Adenosine triphosphate: Click to Expand ⟱
Source:
Type:
Adenosine triphosphate (ATP) is the source of energy for use and storage at the cellular level.
Cellular ATP levels are critical for cell survival, and several reports have shown that reductions in cellular ATP levels can lead to apoptosis and other types of cell death in cancer cells, depending on the level of depletion.
Adenosine triphosphate (ATP) is one of the main biochemical components of the tumor microenvironment (TME), where it can promote tumor progression or tumor suppression depending on its concentration and on the specific ecto-nucleotidases and receptors expressed by immune and cancer cells.

Cancer cells, unlike normal cells, derive as much as 60% of their ATP from glycolysis via the “Warburg effect”, and the remaining 40% is derived from mitochondrial oxidative phosphorylation.
Scientific Papers found: Click to Expand⟱
2656- AL,    Allicin Protects PC12 Cells Against 6-OHDA-Induced Oxidative Stress and Mitochondrial Dysfunction via Regulating Mitochondrial Dynamics
- in-vitro, Park, PC12
*antiOx↑, Allicin, the main biologically active compound derived from garlic, has been shown to exert various anti-oxidative and anti-apoptotic activities in in vitro and in vivo studies.
*Apoptosis↓, allicin treatment significant increased cell viability, and decreased LDH release and apoptotic cell death after 6-OHDA exposure
*LDH↓,
ROS↓, Allicin also inhibited ROS generation
*lipid-P↓, reduced lipid peroxidation and preserved the endogenous antioxidant enzyme activities.
*mtDam↓, These protective effects were associated with suppressed mitochondrial dysfunction,
*MMP↓, as evidenced by decreased MMP collapse and cytochrome c release,
*Cyt‑c↓,
*ATP∅, preserved mitochondrial ATP synthesis,
*Ca+2↝, and the promotion of mitochondrial Ca(2+) buffering capacity
*neuroP↑, allicin treatment can exert protective effects against PD related neuronal injury through inhibiting oxidative stress and mitochondrial dysfunction with dynamic changes.

1355- Ash,    Withaferin A-Induced Apoptosis in Human Breast Cancer Cells Is Mediated by Reactive Oxygen Species
- in-vitro, BC, MDA-MB-231 - in-vitro, BC, MCF-7 - in-vitro, Nor, HMEC
eff↑, WA treatment caused ROS production in MDA-MB-231 and MCF-7 cells, but not in a normal human mammary epithelial cell line (HMEC). ****
mt-ROS↑, WA-induced apoptosis in human breast cancer cells is mediated by mitochondria-derived ROS
mitResp↓,
OXPHOS↓, WA exposure was accompanied by inhibition of oxidative phosphorylation and inhibition of complex III activity.
compIII↑,
BAX↑,
Bak↑,
other↓, Cu,Zn-Superoxide dismutase (Cu,Zn-SOD) overexpression confers protection against WA-induced ROS production and apoptosis
ATP∅, steady-state levels of ATP were unaffected by WA treatment in either cell line
*ROS∅, but not in a normal human mammary epithelial cell line (HMEC). WA treatment caused ROS production in breast cancer cells, HMEC were resistant to pro-oxidant effect of this agent.

2242- MF,    Electromagnetic stimulation increases mitochondrial function in osteogenic cells and promotes bone fracture repair
- in-vitro, Nor, NA
*MMP↑, we show that application of a low intensity constant EM field source on osteogenic cells in vitro resulted in increased mitochondrial membrane potential and respiratory complex I activity and induced osteogenic differentiation.
*Diff↑,
*OXPHOS↑, effect was mediated via increased OxPhos activity
*BMD↑, EM field source enhanced fracture repair via improved biomechanical properties and increased callus bone mineralization
ATP∅, higher mitochondrial OxPhos activity leads to higher ATP production, increased cellular activity leads to increased ATP consumption.


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 ⓘ

OXPHOS↓, 1,   ROS↓, 1,   mt-ROS↑, 1,  

Mitochondria & Bioenergetics ⓘ

ATP∅, 2,   compIII↑, 1,   mitResp↓, 1,  

Cell Death ⓘ

Bak↑, 1,   BAX↑, 1,  

Transcription & Epigenetics ⓘ

other↓, 1,  

Drug Metabolism & Resistance ⓘ

eff↑, 1,  
Total Targets: 10

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 1,   lipid-P↓, 1,   OXPHOS↑, 1,   ROS∅, 1,  

Mitochondria & Bioenergetics ⓘ

ATP∅, 1,   MMP↓, 1,   MMP↑, 1,   mtDam↓, 1,  

Core Metabolism/Glycolysis ⓘ

LDH↓, 1,  

Cell Death ⓘ

Apoptosis↓, 1,   Cyt‑c↓, 1,  

Proliferation, Differentiation & Cell State ⓘ

Diff↑, 1,  

Migration ⓘ

Ca+2↝, 1,  

Clinical Biomarkers ⓘ

BMD↑, 1,   LDH↓, 1,  

Functional Outcomes ⓘ

neuroP↑, 1,  
Total Targets: 16

Scientific Paper Hit Count for: ATP, Adenosine triphosphate
1 Allicin (mainly Garlic)
1 Ashwagandha(Withaferin A)
1 Magnetic Fields
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#:21  State#:%  Dir#:6
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