CTSD Cancer Research Results

CTSD, Cathepsin D: Click to Expand ⟱
Source:
Type:
CTSD — Cathepsin D

Primary role: Lysosomal aspartyl protease; regulator of autophagic degradation and stress-adaptive survival signaling.

Cancer relevance:
CTSD supports lysosomal proteolysis and autophagic completion, enabling metabolic recycling under stress. In cancer, it is often overexpressed and can function both intracellularly (autophagy, apoptosis modulation) and extracellularly (growth factor processing). Partial lysosomal leakage of CTSD contributes to apoptotic signaling, while intact activity promotes therapy resistance.

Net effect in established cancer:
Predominantly pro-survival via maintenance of autophagic flux, with pro-apoptotic potential under severe stress.
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,


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:


Mitochondria & Bioenergetics ⓘ

ATP↓, 1,  

Core Metabolism/Glycolysis ⓘ

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

Autophagy & Lysosomes ⓘ

autoF↓, 1,   lysosome↓, 1,   TumAuto↑, 1,  

DNA Damage & Repair ⓘ

cl‑PARP1↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

CTSB↓, 1,   CTSD↓, 1,   CTSL↑, 1,   TumCG↓, 1,  

Drug Metabolism & Resistance ⓘ

eff↑, 1,  

Clinical Biomarkers ⓘ

p‑LDH↓, 1,  
Total Targets: 15

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: CTSD, Cathepsin D
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#:1430  State#:%  Dir#:1
  wNotes=on  sortOrder:rid,rpid

 

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