autophagy Cancer Research Results

autophagy, autophagy: Click to Expand ⟱
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Autophagy - Macroautophagy / Autophagic-Lysosomal Pathway

Abbreviation: Autophagy, Macroautophagy

Type: Cellular degradation pathway / lysosomal quality-control process

Function: Autophagy is a conserved cellular recycling pathway in which cytoplasmic proteins, damaged organelles, protein aggregates, and other cellular components are enclosed within autophagosomes and delivered to lysosomes for degradation. Major regulators include ULK1/ATG13, BECN1, VPS34, ATG5, ATG7, LC3, p62/SQSTM1, mTOR, and AMPK.

Cancer: ↕ Context-dependent. Autophagy can suppress tumor initiation by removing damaged organelles, limiting oxidative stress, and maintaining genomic stability. In established cancers, however, increased autophagy can support tumor-cell survival during hypoxia, nutrient deprivation, metabolic stress, and anticancer treatment and can contribute to treatment resistance. The biological effect therefore depends strongly on tumor type and disease stage.

Alzheimer's Disease: ↓ / impaired autophagic flux. Alzheimer's disease is characterized by dysfunction of the autophagic-lysosomal pathway, including impaired autophagosome maturation and lysosomal clearance. Defective autophagy contributes to accumulation of amyloid-β, phosphorylated tau, damaged mitochondria, and other abnormal proteins. Restoration of effective autophagic flux is generally considered neuroprotective.
Scientific Papers found: Click to Expand⟱
7837- ISQ,    Isoquercitrin Delays Denervated Soleus Muscle Atrophy by Inhibiting Oxidative Stress and Inflammation
- in-vivo, Nor, NA
*Dose↝, Isoquercitrin demonstrated the optimal protective effect at 20 mg/kg/d, which was the dose used in subsequent experiments.
*autophagy↓, Following isoquercitrin treatment, mitochondrial vacuolation and autophagy were inhibited, as evidenced by reduced level of autophagy-related proteins (ATG7, BNIP3, LC3B, and PINK1);
*ATG7↓,
*BNIP3↓,
*LC3B↓,
*PINK1↓,
*ROS↓, (ROS) in the target muscle was reduced, which might be associated with the upregulation of antioxidant factors (SOD1, SOD2, NRF2, NQO1, and HO1) and the downregulation of ROS production-related factors (Nox2, Nox4, and DUOX1).
*SOD1↑,
*SOD2↑,
*NRF2↑,
*NQO1↑,
*HO-1↑,
*NOX2↓,
*NOX4↓,
*DUOX1↓,
*IL1β↓, isoquercitrin treatment reduced the levels of inflammatory factors—interleukin (IL)-1β, IL-6, and tumor necrosis factor-α (TNF-α)—in the target muscle and inactivated the JAK/STAT3 signaling pathway.
*IL6↓,
*TNF-α↓,
*JAK↓,
*STAT3↓,
*Inflam↓, via inhibition of oxidative stress and inflammatory response.

7831- PCA,  MBS,    Neuroprotective Potential of Mung Bean (Vigna radiata L.) Polyphenols in Alzheimer's Disease: A Review
- Review, AD, NA
*BBB↑, indicating its BBB permeability
*neuroP↑, neuroprotective activity of protocatechuic acid was observed by several animal models
*Aβ↓, Mechanism studies showed that protocatechuic acid inhibited Aβ plaque deposits via multiple ways, such as reduction of Aβ peptides production by inhibiting βsecretase activity, suppression of Aβ aggregation, and destabilization of performed Aβ f
*p‑tau↓, indicated that protocatechuic acid inhibited tau hyperphosphorylation and autophagy induced by okadaic acid through decreasing the activation of GSK-3β
*autophagy↓,
*GSK‐3β↓,
*NeuroI↓, antineuroinflammatory activity as indicated by the reduced neuroinflammatory markers, iNOS, and COX2 in the brain of AD mice.
*iNOS↓,
*COX2/PTGS2↓,
*BDNF↑, protocatechuic acid upregulated the expression of several cytoprotective factors, such as BDNF and myocyte enhancer factor 2D (MEF2D),
*MEF2D↑,
*cognitive↑, upregulated the cytoprotective factors, thus improving the cognitive and memory function of AD rodents.
*memory↑,


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:


NA, unassigned(tgid=0) ⓘ

autophagy↓, 2,   DUOX1↓, 1,   MEF2D↑, 1,   NeuroI↓, 1,   NOX2↓, 1,  

Redox & Oxidative Stress(tgid=1) ⓘ

HO-1↑, 1,   NOX4↓, 1,   NQO1↑, 1,   NRF2↑, 1,   ROS↓, 1,   SOD1↑, 1,   SOD2↑, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

PINK1↓, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

ATG7↓, 1,  

Cell Death(tgid=5) ⓘ

iNOS↓, 1,  

Autophagy & Lysosomes(tgid=9) ⓘ

BNIP3↓, 1,   LC3B↓, 1,  

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

GSK‐3β↓, 1,   STAT3↓, 1,  

Barriers & Transport(tgid=15) ⓘ

BBB↑, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

COX2/PTGS2↓, 1,   IL1β↓, 1,   IL6↓, 1,   Inflam↓, 1,   JAK↓, 1,   TNF-α↓, 1,  

Synaptic & Neurotransmission(tgid=18) ⓘ

BDNF↑, 1,   p‑tau↓, 1,  

Protein Aggregation(tgid=19) ⓘ

Aβ↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

Dose↝, 1,  

Clinical Biomarkers(tgid=22) ⓘ

IL6↓, 1,  

Functional Outcomes(tgid=23) ⓘ

cognitive↑, 1,   memory↑, 1,   neuroP↑, 1,  
Total Targets: 34

Scientific Paper Hit Count for: autophagy, autophagy
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#:1709  State#:%  Dir#:1
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