mitResp Cancer Research Results

mitResp, mitochondrial respiration: Click to Expand ⟱
Source:
Type:
Mitochondrial respiration plays a crucial role in the development and progression of cancer. Cancer cells often exhibit altered metabolic profiles, including changes in mitochondrial respiration, to support their rapid growth and proliferation.

In cancer cells, mitochondrial respiration is often downregulated, and instead, they rely on glycolysis for energy production, even in the presence of oxygen. This phenomenon is known as the "Warburg effect."

There are several key players involved in the regulation of mitochondrial respiration in cancer cells, including:

Pyruvate dehydrogenase (PDH): a critical enzyme that converts pyruvate into acetyl-CoA, which is then fed into the citric acid cycle.
Citrate synthase: an enzyme that catalyzes the first step of the citric acid cycle.
Succinate dehydrogenase (SDH): an enzyme that participates in both the citric acid cycle and the electron transport chain.
Cytochrome c oxidase (COX): the final enzyme in the electron transport chain, responsible for generating ATP.
Alterations in the expression and activity of these enzymes can impact mitochondrial respiration in cancer cells. For example, increased expression of PDH and citrate synthase can enhance mitochondrial respiration, while decreased expression of SDH and COX can impair it.

Additionally, various transcription factors and signaling pathways regulate mitochondrial respiration in cancer cells, including:

HIF-1α (hypoxia-inducible factor 1 alpha): a transcription factor that promotes glycolysis and suppresses mitochondrial respiration in response to hypoxia.
c-Myc: a transcription factor that regulates the expression of genes involved in mitochondrial respiration and biogenesis.
PI3K/Akt/mTOR: a signaling pathway that promotes cell growth and proliferation, in part by regulating mitochondrial respiration.
NA, Not Available: Click to Expand ⟱
none (reserved)
Scientific Papers found: Click to Expand⟱
2879- HNK,    Honokiol Inhibits Lung Tumorigenesis through Inhibition of Mitochondrial Function
- in-vitro, Lung, H226 - in-vivo, NA, NA
tumCV↓, selectivity↑, TumCP↓, TumCCA↑, Apoptosis↑, mt-ROS↑, Casp3↑, Casp7↑, OCR↓, Cyt‑c↑, ATP↓, mitResp↓, AMP↑, AMPK↑,

Showing Research Papers: 1 to 1 of 1

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 1

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

mt-ROS↑, 1,  

Mitochondria & Bioenergetics ⓘ

ATP↓, 1,   mitResp↓, 1,   OCR↓, 1,  

Core Metabolism/Glycolysis ⓘ

AMP↑, 1,   AMPK↑, 1,  

Cell Death ⓘ

Apoptosis↑, 1,   Casp3↑, 1,   Casp7↑, 1,   Cyt‑c↑, 1,  

Transcription & Epigenetics ⓘ

tumCV↓, 1,  

Cell Cycle & Senescence ⓘ

TumCCA↑, 1,  

Migration ⓘ

TumCP↓, 1,  

Drug Metabolism & Resistance ⓘ

selectivity↑, 1,  
Total Targets: 14

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: mitResp, mitochondrial respiration
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:0  Cells:%  prod#:%  Target#:952  State#:%  Dir#:1
  wNotes=0  sortOrder:rid,rpid

 

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