Morin / compV Cancer Research Results

MOR, Morin: Click to Expand ⟱
Features:

Morin - 2',3,4',5,7-Pentahydroxyflavone

Recommended Abbreviation: MOR

Type: Flavonol / polyphenolic flavonoid

Sources: Morin occurs naturally in several plants and foods, including members of Morus, Maclura, Artocarpus, and Psidium species.

Function: Morin is a polyphenolic flavonol with antioxidant, anti-inflammatory, metabolic, neuroprotective, and antiproliferative activities. It modulates oxidative stress, mitochondrial function, inflammatory signaling, apoptosis, cell-cycle regulation, and signaling pathways including NF-κB, STAT3, PI3K/AKT, MAPK, and GSK-3β.

Cancer: Preclinical studies show broad anticancer activity. Morin can inhibit proliferation, migration, invasion, epithelial-mesenchymal transition, inflammatory signaling, and angiogenic pathways while promoting apoptosis and cell-cycle arrest. Reported molecular pathways include STAT3, NF-κB, PI3K/AKT, MAPK, Hippo, MMPs, and ROS-related signaling. Human anticancer efficacy has not been established.

Alzheimer's Disease: Preclinical evidence suggests neuroprotective activity. Morin can reduce amyloid-β-induced oxidative stress, mitochondrial dysfunction, calcium dysregulation, and neuronal injury and may inhibit GSK-3β-related signaling relevant to tau hyperphosphorylation and amyloid pathology. Evidence remains experimental, with no established clinical efficacy for Alzheimer's disease.
compV, Mitochondrial Complex V: Click to Expand ⟱
Source:
Type:

Mitochondrial Complex V - ATP Synthase / F1Fo ATP Synthase

Abbreviation: Complex V, ATP synthase, F1Fo-ATP synthase

Type: Mitochondrial oxidative phosphorylation complex / ATP-producing enzyme complex

Function: Mitochondrial Complex V is the ATP synthase of the inner mitochondrial membrane. It uses the proton-motive force generated by respiratory-chain Complexes I, III, and IV to phosphorylate ADP to ATP. Complex V consists of a membrane-embedded Fo proton-translocation domain and a matrix-facing F1 catalytic domain and is composed of multiple nuclear- and mitochondrial-encoded subunits.

Cancer: ↕ Context-dependent. Complex V activity and expression are altered during cancer metabolic reprogramming. Tumors dependent on oxidative phosphorylation may maintain or increase ATP synthase activity to support ATP production, growth, survival, and treatment resistance, whereas glycolytic tumors may show reduced oxidative-phosphorylation activity. Individual ATP synthase subunits can display tumor-specific increases or decreases.

Alzheimer's Disease: ↓ Impaired mitochondrial Complex V activity and ATP production are associated with Alzheimer's disease. Altered ATP synthase subunit expression, oxidative damage, mitochondrial membrane dysfunction, and reduced oxidative phosphorylation contribute to cellular energy failure, synaptic dysfunction, and neuronal vulnerability.
Scientific Papers found: Click to Expand⟱
7817- ISQ,  MOR,    Morin and isoquercitrin protect against ischemic neuronal injury by modulating signaling pathways and stimulating mitochondrial biogenesis
- in-vitro, AD, NA
*neuroP?, *compI↑, *compIII↑, *compV↑, *p‑ERK↑,

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:


Total Targets: 0

Pathway results for Effect on Normal Cells:


NA, unassigned(tgid=0) ⓘ

compV↑, 1,  

Redox & Oxidative Stress(tgid=1) ⓘ

compI↑, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

compIII↑, 1,  

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

p‑ERK↑, 1,  

Functional Outcomes(tgid=23) ⓘ

neuroP?, 1,  
Total Targets: 5

Scientific Paper Hit Count for: compV, Mitochondrial Complex V
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#:460  Target#:1701  State#:%  Dir#:%
  wNotes=0  sortOrder:rid,rpid

 

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