CTSB Cancer Research Results

CTSB, Cathepsin B: Click to Expand ⟱
Source:
Type:
CTSB — Cathepsin B

Primary role: Lysosomal cysteine protease; executor of late-stage autophagic flux and mediator of lysosome-dependent cell death.

Cancer relevance:
CTSB is frequently overexpressed and mislocalized in cancer. In intact lysosomes, it enables productive autophagic flux by degrading autophagic cargo. Upon lysosomal membrane permeabilization (LMP), CTSB is released into the cytosol where it activates apoptotic signaling (including caspase-dependent and independent pathways). Extracellular CTSB promotes ECM degradation, invasion, and metastasis.

Net effect in established cancer:
Context-dependent, but predominantly pro-tumor via invasion and survival; pro-death when lysosomal integrity is lost.


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,

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 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:


Mitochondria & Bioenergetics

ATP↓, 1,  

Core Metabolism/Glycolysis

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

Transcription & Epigenetics

other↓, 1,  

Autophagy & Lysosomes

autoF↓, 2,   LC3II↑, 1,   lysosome↓, 2,   TumAuto↓, 1,   TumAuto↑, 1,  

DNA Damage & Repair

cl‑PARP1↑, 1,  

Proliferation, Differentiation & Cell State

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

Immune & Inflammatory Signaling

CTSZ↓, 1,  

Drug Metabolism & Resistance

eff↑, 1,  

Clinical Biomarkers

p‑LDH↓, 1,  
Total Targets: 22

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: CTSB, Cathepsin B
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#:1429  State#:%  Dir#:1
wNotes=on sortOrder:rid,rpid

 

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