Component
Cytostatic autophagy in breast cancer cells
Autophagy associated with growth arrest rather than cytotoxic killing.
1 recorded relationships. Experimental role, claim status and evidence remain attached to each record.
How nutrients influence it
Every nutrient with a recorded effect on this component, credited to the nutrient that acted rather than the chapter that recorded it. Open a nutrient to see the findings and the conditions they were measured under.
Other things that act on it
Enzymes, hormones, genes, and other components with a recorded effect. These are not nutrients, so they do not count toward the arrows above. Each finding names the chapter that recorded it.
How nutrients reach it in more than one step
Chains of two or more recorded steps that end here, grouped by the nutrient they start from. Each step is a separate finding, so a chain is a route a mechanism could take, not proof that it does.
Tracing routes…
What it does
Every recorded relationship this component is part of, grouped by its role. Plain wording comes first; the technical statement follows.
Where it participates (unsigned role)
Ivermectin decreased PAK1 through ubiquitination-mediated degradation, lowering Akt phosphorylation and blocking Akt/mTOR signalling, which produced cytostatic autophagy in breast cancer cells.
Experimental context and source evidence
- duration
- Not stated here
- evidence_access
- Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
- experimental_model
- Human breast cancer cells and breast cancer xenografts
- exposure
- Ivermectin
- limitations
- The autophagy described is cytostatic and associated with suppressed tumour growth rather than cytotoxic killing.
- organism
- Human breast cancer cells and breast cancer xenografts
- plain_language
- Ivermectin decreased PAK1 through ubiquitination-mediated degradation, lowering Akt phosphorylation and blocking Akt/mTOR signalling, which produced cytostatic autophagy in breast cancer cells.
- primary_references
- Ivermectin Induces Cytostatic Autophagy by Blocking the PAK1/Akt Axis in Breast Cancer. (2016). https://pubmed.ncbi.nlm.nih.gov/27302166/ DOI: 10.1158/0008-5472.CAN-15-2887
- route
- In vitro and in vivo xenograft
- tissue
- PAK1 abundance, Akt phosphorylation and autophagy
Ivermectin: mechanism of action across parasite, host barrier and mammalian targets (2026-09-22) · lines 211–220
Original AI-assisted curation of sixteen primary studies resolved by PubMed title search and cross-checked against live PubMed metadata. Study-specific citations, concentrations, negative findings and limitations retained. Not publisher full text. · supports · · source_derived_draft · unverified_draft
## ivermectin-pak1-akt-autophagy Ivermectin decreased PAK1 through ubiquitination-mediated degradation, lowering Akt phosphorylation and blocking Akt/mTOR signalling, which produced cytostatic autophagy in breast cancer cells. Model/species: Human breast cancer cells and breast cancer xenografts Tissue/system: PAK1 abundance, Akt phosphorylation and autophagy Exposure: Ivermectin Route: In vitro and in vivo xenograft Duration: Not stated here Limits: The autophagy described is cytostatic and associated with suppressed tumour growth rather than cytotoxic killing. Primary reference: Ivermectin Induces Cytostatic Autophagy by Blocking the PAK1/Akt Axis in Breast Cancer. (2016). https://pubmed.ncbi.nlm.nih.gov/27302166/ DOI: 10.1158/0008-5472.CAN-15-2887 Access: Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
Complete structured claim and evidence
The events it takes part in
A mechanism often involves more than two components. These are the full events, with every participant and its role.
Situations it appears in
Low-supply and faulty-machinery situations recorded in the chapters where this component plays a part.
In the sources
Preserved passages that mention this component, quoted exactly. Open one to read it in context.
Open hypotheses
Proposed ideas that involve this component. They are labeled as hypotheses and do not change any recorded statement.
This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.