ECAR Cancer Research Results

ECAR, Extracellular Acidification Rate: Click to Expand ⟱
Source:
Type:
ECAR (Extracellular Acidification Rate) is a measure of the rate at which cells release acidic byproducts, such as lactic acid, into the extracellular environment. In the context of cancer, ECAR is often used as a proxy for glycolytic activity, as cancer cells often exhibit increased glycolysis, even in the presence of oxygen.

Studies have shown that cancer cells often have a higher ECAR compared to normal cells, indicating that they are producing more acidic byproducts. This is thought to be due to the fact that cancer cells often rely more heavily on glycolysis for energy production, even in the presence of oxygen.
-ECAR reflects the glycolysis activity
Scientific Papers found: Click to Expand⟱
2389- BA,    Baicalin alleviates lipid accumulation in adipocytes via inducing metabolic reprogramming and targeting Adenosine A1 receptor
- in-vitro, Obesity, 3T3
*ECAR↑, Baicalin promoted metabolic reprogramming in 3T3-L1 preadipocytes, characterized by increased ECAR and decreased OCR
*OCR↓,
*p‑AMPK↑, baicalin significantly altered cellular respiration by reducing mitochondrial oxygen consumption while enhancing glycolytic flux, accompanied by increased phosphorylation of AMPK and ACC, suggesting an adaptation to altered energy availability.
*p‑ACC↑,
*Glycolysis↑, significant enrichment in metabolic pathways such as glycolysis, gluconeogenesis, and lipid metabolism.
*lipidDe↓, inhibited the maturation of sterol regulatory element binding protein 1 (SREBP1) and finally alleviated lipid deposition.
*SREBP1↓,
*FAO↑, baicalin induces metabolic reprogramming of adipocytes by inhibiting glucose aerobic metabolism while enhancing anaerobic glycolysis and FAO.
*HK2↑, baicalin upregulated glycolytic enzymes, such as HK1, HK2, PKM2, and LDHA, while downregulating pyruvate dehydrogenase,
*PKM2↑,
*LDHA↑,
*PDKs↓,
*ACC↓, leading to decreased acetyl-CoA production and enhanced fatty acid β-oxidation.

4355- MF,    Ambient and supplemental magnetic fields promote myogenesis via a TRPC1-mitochondrial axis: evidence of a magnetic mitohormetic mechanism
- in-vitro, Nor, C2C12
*mt-OCR↑, figure 1
*mt-ROS↑, Exposure to PEMFs stimulated the production of ROS (Fig. 6A, B) and ATP
*ECAR↑, figure 6
*Dose↝, barrages of 20 × 150 μs on and off pulses for 6 ms repeated at a frequency of 15 Hz. The magnetic flux density rose to predetermined maximal level within ∼50 μs (∼17 T/s) when driving field amplitudes between 0.5 and 3 mT.
*Ca+2↑, 10 min) of C2C12 myoblasts to PEMFs (Supplemental Fig. S1A) augmented cytosolic calcium levels [intracellular [Ca2+] concentration ([Ca2+]i), blue] relative to unexposed myoblasts
*ATP↑,
*other↑, PEMF-stimulated proliferation of myoblasts
*eff↓, TRPC1 silencing precludes PEMF sensitivity.
*eff↝, revealed a magnetic efficacy window


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:


Total Targets: 0

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

lipidDe↓, 1,   mt-ROS↑, 1,  

Mitochondria & Bioenergetics ⓘ

ATP↑, 1,   OCR↓, 1,   mt-OCR↑, 1,  

Core Metabolism/Glycolysis ⓘ

ACC↓, 1,   p‑ACC↑, 1,   p‑AMPK↑, 1,   ECAR↑, 2,   FAO↑, 1,   Glycolysis↑, 1,   HK2↑, 1,   LDHA↑, 1,   PDKs↓, 1,   PKM2↑, 1,   SREBP1↓, 1,  

Transcription & Epigenetics ⓘ

other↑, 1,  

Migration ⓘ

Ca+2↑, 1,  

Drug Metabolism & Resistance ⓘ

Dose↝, 1,   eff↓, 1,   eff↝, 1,  
Total Targets: 21

Scientific Paper Hit Count for: ECAR, Extracellular Acidification Rate
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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