CTSL Cancer Research Results

CTSL, Cathepsin L: Click to Expand ⟱
Source:
Type:
CTSL — Cathepsin L

Primary role: Lysosomal and nuclear cysteine protease; regulator of autophagy, transcriptional programs, and cellular plasticity.

Cancer relevance:
CTSL is linked to high autophagic flux, EMT, and stem-like phenotypes. Beyond lysosomes, CTSL can translocate to the nucleus and influence transcription factor processing, supporting dedifferentiation and invasiveness. It also contributes to ECM remodeling and metastatic dissemination.

Net effect in established cancer:
Strongly pro-tumor, supporting autophagy-dependent survival, EMT, and metastasis.
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: CTSL, Cathepsin L
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#:1431  State#:%  Dir#:2
  wNotes=on  sortOrder:rid,rpid

 

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