compIII Cancer Research Results

compIII, Mitochondrial complex III: Click to Expand ⟱
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Type:
Complex III is part of the mitochondrial respiratory chain. It plays a key role in oxidative phosphorylation by transferring electrons from ubiquinol (coenzyme Q) to cytochrome c.
• The complex is made up of multiple subunits. In humans, some of the key proteins include:
-UQCRC1 (ubiquinol-cytochrome c reductase core protein I)
-UQCRC2 (core protein II)
-UQCRFS1 (the Rieske iron-sulfur protein)
-UQCRB (cytochrome b)

Complex III is a significant source of reactive oxygen species (ROS) when electron transport is inefficient. Increased ROS can promote DNA damage and genomic instability, factors known to drive cancer progression.
Expression levels of Complex III subunits, particularly UQCRFS1 and UQCRC1, have been evaluated as biomarkers. High expression may suggest a more aggressive tumor phenotype, thus linking mitochondrial respiratory chain activity with clinical outcomes.
Scientific Papers found: Click to Expand⟱
2014- CAP,    Role of Mitochondrial Electron Transport Chain Complexes in Capsaicin Mediated Oxidative Stress Leading to Apoptosis in Pancreatic Cancer Cells
- in-vitro, PC, Bxpc-3 - in-vitro, Nor, HPDE-6 - in-vivo, PC, AsPC-1
ROS↑, ROS was about 4–6 fold more as compared to control and as early as 1 h after capsaicin treatment in BxPC-3 and AsPC-1 cells
*ROS∅, but not in normal HPDE-6 cells
selectivity↑, only small ~1.2fold ROS increase in normal cell
compI↓, capsaicin inhibits about 2.5–9% and 5–20% of complex-I activity
compIII↓, and 8–75% of complex-III activity in BxPC-3 and AsPC-1 cells respectively
eff↑, which was attenuable by SOD, catalase and EUK-134.
selectivity↑, capsaicin treatment failed to inhibit complex-I or complex-III activities in normal HPDE-6 cells
ATP↓, ATP levels were drastically suppressed by capsaicin treatment in both BxPC-3 and AsPC-1 cells
Cyt‑c↑, release of cytochrome c and cleavage of both caspase-9 and caspase-3 due to disruption of mitochondrial membrane potential
Casp9↑,
Casp3↑,
MMP↓,
SOD↓, mice orally fed with 2.5 mg/kg capsaicin show decreased SOD activity and an increase in GSSG/GSH levels as compared to controls
GSH/GSSG↓, mice orally fed with 2.5 mg/kg capsaicin
Apoptosis↑, Capsaicin triggers apoptosis in pancreatic cancer cells but not in normal HPDE-6 cells
*toxicity∅, Capsaicin triggers apoptosis in pancreatic cancer cells but not in normal HPDE-6 cells
GSH↓, Taken together, our results suggest that depletion of GSH level and inhibition of SOD, catalase and GPx by capsaicin disturbs the cellular redox homeostasis resulting in increased oxidative stress.
Catalase↓,
GPx↓,
Dose↝, 13.2 mg dose of capsaicin for a 60 kg person

6699- DFC,    Mitochondrial H2O2 Is a Central Mediator of Diclofenac-Induced Hepatocellular Injury
- vitro+vivo, Nor, NA
*ROS↑, The detrimental hepatotoxicity of diclofenac, a widely used NSAID, is primarily connected to oxidative damage in mitochondria, which are the primary source of reactive oxygen species (ROS).
*hepatoP↓, diclofenac’s harmful hepatotoxicity is primarily related to the effects of ROS on mitochondria
*eff↑, PrxIII or other antioxidants targeting mitochondrial H2O2 could be explored as potential therapeutic agents to protect against the hepatotoxicity associated with NSAID use.
*ATP↓, diclofenac and metabolites impede ATP production and oxidative phosphorylation in rat liver mitochondria
OXPHOS↓,
*ETC↓, diclofenac inhibits the electron transport chain (ETC) complexes I and III, which could thereby lead to electron leakage from the respiratory chain, slowing mitochondrial respiration
*compI↓,
*compIII↓,

6698- DFC,    Diclofenac induces proteasome and mitochondrial dysfunction in murine cardiomyocytes and hearts
- in-vivo, Nor, NA
*cardioP↓, One of the most common nonsteroidal anti-inflammatory drugs (NSAIDs) used worldwide, diclofenac (DIC), has been linked to increased risk of cardiovascular disease (CVD)
*ROS↑, DIC increased ROS production and cell death in H9c2 cells
MMP↓, DIC inhibited mitochondrial Complex III, a major source of ROS, and impaired mitochondrial membrane potential suggesting that mitochondria are the major sites of ROS generation.
compIII↓,


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(tgid=1) ⓘ

Catalase↓, 1,   compI↓, 1,   GPx↓, 1,   GSH↓, 1,   GSH/GSSG↓, 1,   OXPHOS↓, 1,   ROS↑, 1,   SOD↓, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

ATP↓, 1,   compIII↓, 2,   MMP↓, 2,  

Cell Death(tgid=5) ⓘ

Apoptosis↑, 1,   Casp3↑, 1,   Casp9↑, 1,   Cyt‑c↑, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

Dose↝, 1,   eff↑, 1,   selectivity↑, 2,  
Total Targets: 18

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

compI↓, 1,   ROS↑, 2,   ROS∅, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

ATP↓, 1,   compIII↓, 1,   ETC↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

eff↑, 1,  

Functional Outcomes(tgid=23) ⓘ

cardioP↓, 1,   hepatoP↓, 1,   toxicity∅, 1,  
Total Targets: 10

Scientific Paper Hit Count for: compIII, Mitochondrial complex III
2 Diclofenac
1 Capsaicin
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#:1070  State#:%  Dir#:1
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