ECAR Cancer Research Results

ECAR, Extracellular Acidification Rate: Click to Expand ⟱
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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⟱
1574- Citrate,    Citrate Suppresses Tumor Growth in Multiple Models through Inhibition of Glycolysis, the Tricarboxylic Acid Cycle and the IGF-1R Pathway
- in-vitro, Lung, A549 - in-vitro, Melanoma, WM983B - in-vivo, NA, NA
TumCG↓,
eff↑, additional benefit accrued in combination with cisplatin
T-Cell↑, significantly higher infiltrating T-cells
p‑IGF-1R↓, citrate inhibited IGF-1R phosphorylation
p‑Akt↓, inhibited AKT phosphorylation
PTEN↑, activated PTEN
p‑eIF2α↑, increased expression of p-eIF2a p-eIF2a was decreased when PTEN was depleted
OCR↓, citrate treatment of A549 cells dramatically reduced oxygen consumption
ROS↓, observed a decrease in ROS in A549
ECAR∅, acidification rate (ECAR) and found it to be unchanged
IL1↑, s (e.g. interleukin-1, tumor necrosis factor-alpha, etc) and anti-inflammatory cytokines (e.g. interleukin-10 and interleukin 1 receptor antagonist) are activated
TNF-α↑,
IL10↑,
IGF-1R↓, Citrate Inhibits IGF-1R Activation And Its Downstream Pathway
eIF2α↑, eIF2α activity was increased in A549 cells after citrate treatment
PTEN↑, PTEN was activated
TCA↓,
Glycolysis↓, citrate may inhibit tumor growth via inhibiting glycolysis and the TCA cycle and that this effect appears to be selective to tumor tissue.
selectivity↑, citrate may inhibit tumor growth via inhibiting glycolysis and the TCA cycle and that this effect appears to be selective to tumor tissue.
*toxicity∅, Chronic citrate treatment was non-toxic as evidenced by gross pathology in numerous organs (liver, lung, spleen and kidney)
Dose∅, corresponding to approximately 56 g of citrate in a 70 kg person

993- RES,    Resveratrol reverses the Warburg effect by targeting the pyruvate dehydrogenase complex in colon cancer cells
- in-vitro, CRC, Caco-2 - in-vivo, Nor, HCEC 1CT
TumCG↓,
Glycolysis↓,
PPP↓,
ATP↑, significant increase (20%) in ATP production
PDH↑, Resveratrol targets the pyruvate dehydrogenase (PDH) complex, a key mitochondrial gatekeeper of energy metabolism, leading to an enhanced PDH activity.
Ca+2↝, resveratrol is a potent modulator of many cellular Ca2+ signaling pathways. Ca2+ is a key mediator of the effect of resveratrol on the oxidative capacity of colon cancer cells.
TumCP↓,
lactateProd↓,
OCR↑, increase of oxygen consumption rate (OCR) both in normal colonic epithelial HCEC 1CT cells
ECAR↓, Following treatment with resveratrol (10 µM, 48 hr), the ECAR was unchanged in normal HCEC 1CT cells, whereas it was significantly reduced (31%) in HCEC 1CT RPA cells ****
*ECAR∅, Following treatment with resveratrol (10 µM, 48 hr), the ECAR was unchanged in normal HCEC 1CT cells
*other?, Resveratrol promotes a shift from respiration to glycolysis in cancer-like cells, but not in normal colonocytes
cycE/CCNE↑, Resveratrol inhibited cell cycle progression by enhancing the levels of cyclin E and cyclin A
cycA1/CCNA1↑,
TumCCA↑,
cycD1/CCND1↑, and by decreasing cyclin D1
OXPHOS↑, Taken together, these observations indicate that exposure to resveratrol leads to a metabolic reorientation from aerobic glycolysis toward OXPHOS.


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 ⓘ

OXPHOS↑, 1,   ROS↓, 1,  

Mitochondria & Bioenergetics ⓘ

ATP↑, 1,   OCR↓, 1,   OCR↑, 1,  

Core Metabolism/Glycolysis ⓘ

ECAR↓, 1,   ECAR∅, 1,   Glycolysis↓, 2,   lactateProd↓, 1,   PDH↑, 1,   PPP↓, 1,   TCA↓, 1,  

Cell Death ⓘ

p‑Akt↓, 1,  

Protein Folding & ER Stress ⓘ

eIF2α↑, 1,   p‑eIF2α↑, 1,  

Cell Cycle & Senescence ⓘ

cycA1/CCNA1↑, 1,   cycD1/CCND1↑, 1,   cycE/CCNE↑, 1,   TumCCA↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

IGF-1R↓, 1,   p‑IGF-1R↓, 1,   PTEN↑, 2,   TumCG↓, 2,  

Migration ⓘ

Ca+2↝, 1,   TumCP↓, 1,  

Immune & Inflammatory Signaling ⓘ

IL1↑, 1,   IL10↑, 1,   T-Cell↑, 1,   TNF-α↑, 1,  

Drug Metabolism & Resistance ⓘ

Dose∅, 1,   eff↑, 1,   selectivity↑, 1,  
Total Targets: 32

Pathway results for Effect on Normal Cells:


Core Metabolism/Glycolysis ⓘ

ECAR∅, 1,  

Transcription & Epigenetics ⓘ

other?, 1,  

Functional Outcomes ⓘ

toxicity∅, 1,  
Total Targets: 3

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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