autoF Cancer Research Results

autoF, Autophagic flux: Click to Expand ⟱
Source:
Type:
Autophagic flux refers to the entire, dynamic throughput of the autophagy pathway—from autophagosome initiation, cargo sequestration, lysosomal fusion, to final degradation and recycling. In cancer biology, flux (not static autophagy markers) determines whether autophagy is tumor-suppressive or tumor-supportive.
Scientific Papers found: Click to Expand⟱
5173- Ash,  2DG,    Withaferin A inhibits lysosomal activity to block autophagic flux and induces apoptosis via energetic impairment in breast cancer cells
- in-vitro, BC, MCF-7 - in-vitro, BC, MDA-MB-231 - in-vitro, BC, MDA-MB-468 - in-vitro, BC, T47D
autoF↓, WFA blocks autophagy flux and lysosomal proteolytic activity in breast cancer cells.
lysosome↓, WFA treatment inhibits lysosomal activity
TumAuto↑, WFA increases accumulation of autophagosomes, LC3B-II conversion, expression of autophagy-related proteins and autophagosome/lysosome fusion.
p‑LDH↓, WFA decreases expression and phosphorylation of lactate dehydrogenase, the key enzyme that catalyzes pyruvate-to-lactate conversion
ATP↓, reduces adenosine triphosphate levels and increases AMP-activated protein kinase (AMPK) activation.
AMPK↑,
eff↑, WFA and 2-deoxy-d-glucose combination elicits synergistic inhibition of breast cancer cells.
TumCG↓, WFA inhibits breast cancer growth and increases intracellular autophagosomes and autophagy markers
CTSD↓, we found that WFA impaired the maturation of Cathepsin D (CTSD)
CTSB↓, Inhibition of CTSD maturation also indicated reduced CTSB and CTSL activity as they are essential for the cleavage of CTSD.
CTSL↑,
cl‑PARP1↑, WFA and 2-DG treatment also showed higher cleavage of PARP1 in breast cancer cells
LDHA↓, WFA treatment effectively reduces the expression of LDHA in breast cancer cells
TCA↓, d leads to insufficient substrates for TCA cycle,

5125- Sal,    Salinomycin induced ROS results in abortive autophagy and leads to regulated necrosis in glioblastoma
- in-vitro, GBM, NA
ER Stress↑, SLM induces a potent endoplasmic reticulum (ER) stress followed by the trigger of the unfolded protein response (UPR) and an aberrant autophagic flux that culminated in necrosis due to mitochondria and lysosomal alterations.
UPR↑,
autoF↓, SLM treatment does not trigger apoptosis and blocks the autophagy flux in glioma cell line
lysosome↝,
ROS↑, aberrant autophagic flux was orchestrated by the production of Reactive Oxygen Species (ROS)
lipid-P↑, our data suggest that in our system the oxidative stress blocks the autophagic flux through lipid oxidation.
CSCs↓, SLM induces a potent antitumor effect in brain tumor stem cells (BTSCs) and established adult and pediatric glioma cell lines in vitro
necrosis↑, SLM induces necrosis cell death
ATP↓, with increasing doses of SLM displayed a decrease in intracellular ATP levels
MMP↓, SLM treated cells displayed significantly lower ΔΨm than untreated cells
MOMP↑, SLM induces mitochondrial MOMP.
DNAdam↑, We observed double strand breaks in SLM-treated cells (Figure 4C) and it is possible that this DNA damage is induced as a consequence of AIF internalization.
AIF↑,
lysoMP↑, hypothesis that SLM treatment triggers an autophagic process that cannot proceed adequately because of LMP resulting from oxidative stress.
MitoP↑, In addition, impairment of mitochondrial activity would trigger mitophagy, with engulfment of the organelle and initiation of autophagy.
Ca+2↑, The elevated levels of calcium and ROS inside mitochondria results in MOMP

5124- Sal,    Inhibition of the autophagic flux by salinomycin in breast cancer stem-like/progenitor cells interferes with their maintenance
- in-vitro, BC, NA
CSCs↓, Salinomycin (Sal), a K+/H+ ionophore, has recently been shown to be at least 100 times more effective than paclitaxel in reducing the proportion of breast CSCs
LC3II↑, Sal-induced accumulation of LC3-II
other↓, Sal inhibits autophagy flux
lysosome↓, Sal treatment inhibits lysosomal activity
CTSZ↓, The combined activity of cathepsins Z, B, L, and S was significantly lower in Sal–treated cells, as were the specific activities of CTSB and CTSL, indicating that Sal significantly inhibits the activity of cathepsins
CTSB↓,
CTSL↓,
CTSS↓,
autoF↓, Inhibition of the autophagic flux by salinomycin
TumAuto↓, In this study, we reported the inhibitory effect of Sal on autophagy and its consequence on the crosstalk with the apoptosis pathway.


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 ⓘ

lipid-P↑, 1,   ROS↑, 1,  

Mitochondria & Bioenergetics ⓘ

AIF↑, 1,   ATP↓, 2,   MMP↓, 1,  

Core Metabolism/Glycolysis ⓘ

AMPK↑, 1,   p‑LDH↓, 1,   LDHA↓, 1,   TCA↓, 1,  

Cell Death ⓘ

lysoMP↑, 1,   MOMP↑, 1,   necrosis↑, 1,  

Transcription & Epigenetics ⓘ

other↓, 1,  

Protein Folding & ER Stress ⓘ

ER Stress↑, 1,   UPR↑, 1,  

Autophagy & Lysosomes ⓘ

autoF↓, 3,   LC3II↑, 1,   lysosome↓, 2,   lysosome↝, 1,   MitoP↑, 1,   TumAuto↓, 1,   TumAuto↑, 1,  

DNA Damage & Repair ⓘ

DNAdam↑, 1,   cl‑PARP1↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

CSCs↓, 2,   CTSB↓, 2,   CTSD↓, 1,   CTSL↓, 1,   CTSL↑, 1,   CTSS↓, 1,   TumCG↓, 1,  

Migration ⓘ

Ca+2↑, 1,  

Immune & Inflammatory Signaling ⓘ

CTSZ↓, 1,  

Drug Metabolism & Resistance ⓘ

eff↑, 1,  

Clinical Biomarkers ⓘ

p‑LDH↓, 1,  
Total Targets: 35

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: autoF, Autophagic flux
2 salinomycin
1 Ashwagandha(Withaferin A)
1 2-DeoxyGlucose
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#:1433  State#:%  Dir#:1
  wNotes=on  sortOrder:rid,rpid

 

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