Component
Human NSCLC ferroptotic response during cucurbitacin B exposure
Context-specific entity; species, compartment and exposure are stated on each claim.
2 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.
What acts on it
In human H358 and A549 cells, deferoxamine, ferrostatin-1 and liproxstatin-1 reversed cucurbitacin B growth inhibition, supporting a ferroptotic component.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Human NSCLC cell experiments.
- limitations
- Rescue does not establish exclusive cell-death causation or clinical cancer efficacy.
- nutrient_topic
- Cucurbitacins collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Cucurbitacins
- plain_language
- Iron chelation and lipid-radical inhibitors changed the outcome.
- primary_references
- Cucurbitacin B targets STAT3 to induce ferroptosis in non-small cell lung cancer. · 2024 · https://pubmed.ncbi.nlm.nih.gov/38950838/ · DOI 10.1016/j.ejphar.2024.176805
Cucurbitacins: thiol chemistry, cytoskeleton, metabolic dependencies and signaling (2026-09-20) · lines 252–258
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human NSCLC cell experiments. · source_derived_draft · unverified_draft
## cucurbitacin-b-ferroptosis-rescue Iron chelation and lipid-radical inhibitors changed the outcome. In human H358 and A549 cells, deferoxamine, ferrostatin-1 and liproxstatin-1 reversed cucurbitacin B growth inhibition, supporting a ferroptotic component. Model: Human NSCLC cell experiments. Limitations: Rescue does not establish exclusive cell-death causation or clinical cancer efficacy. Evidence access: Primary abstract Cucurbitacin B targets STAT3 to induce ferroptosis in non-small cell lung cancer. · 2024 · https://pubmed.ncbi.nlm.nih.gov/38950838/ · DOI 10.1016/j.ejphar.2024.176805
Complete structured claim and evidence
Where it participates (unsigned role)
STAT3 overexpression reversed tested cucurbitacin B-associated lipid ROS and iron changes, whereas STAT3 silencing enhanced them.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence_access
- Primary abstract
- experimental_model
- Human H358/A549 genetic perturbation experiments.
- limitations
- This establishes model-specific pathway involvement, not universal STAT3 control of ferroptosis.
- nutrient_topic
- Cucurbitacins collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Cucurbitacins
- plain_language
- Changing a signaling protein altered the iron-dependent response.
- primary_references
- Cucurbitacin B targets STAT3 to induce ferroptosis in non-small cell lung cancer. · 2024 · https://pubmed.ncbi.nlm.nih.gov/38950838/ · DOI 10.1016/j.ejphar.2024.176805
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Cucurbitacins: thiol chemistry, cytoskeleton, metabolic dependencies and signaling (2026-09-20) · lines 276–282
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human H358/A549 genetic perturbation experiments. · source_derived_draft · unverified_draft
## cucurbitacin-b-stat3-rescue Changing a signaling protein altered the iron-dependent response. STAT3 overexpression reversed tested cucurbitacin B-associated lipid ROS and iron changes, whereas STAT3 silencing enhanced them. Model: Human H358/A549 genetic perturbation experiments. Limitations: This establishes model-specific pathway involvement, not universal STAT3 control of ferroptosis. Evidence access: Primary abstract Cucurbitacin B targets STAT3 to induce ferroptosis in non-small cell lung cancer. · 2024 · https://pubmed.ncbi.nlm.nih.gov/38950838/ · DOI 10.1016/j.ejphar.2024.176805
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.