Component
Human NSCLC cytotoxic response to cucurbitacin B
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
Pretreating human NSCLC cells with the glutathione-synthesis inhibitor BSO increased cucurbitacin B cytotoxicity.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence_access
- Primary abstract
- experimental_model
- Pharmacological inhibition in human cancer-cell experiments; dose/duration not in accessed abstract.
- limitations
- Experimental synthesis inhibition is not a dietary cucurbitacin deficiency or evidence that oral glutathione protects people.
- nutrient_topic
- Cucurbitacins collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Cucurbitacins
- plain_language
- Weakening glutathione production increased sensitivity in this model.
- primary_references
- Cucurbitacin B potently suppresses non-small-cell lung cancer growth: identification of intracellular thiols as critical targets. · 2013 · https://pubmed.ncbi.nlm.nih.gov/23340170/ · DOI 10.1016/j.canlet.2013.01.008
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Cucurbitacins: thiol chemistry, cytoskeleton, metabolic dependencies and signaling (2026-09-20) · lines 140–146
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Pharmacological inhibition in human cancer-cell experiments; dose/duration not in accessed abstract. · source_derived_draft · unverified_draft
## cucurbitacin-b-bso-sensitivity Weakening glutathione production increased sensitivity in this model. Pretreating human NSCLC cells with the glutathione-synthesis inhibitor BSO increased cucurbitacin B cytotoxicity. Model: Pharmacological inhibition in human cancer-cell experiments; dose/duration not in accessed abstract. Limitations: Experimental synthesis inhibition is not a dietary cucurbitacin deficiency or evidence that oral glutathione protects people. Evidence access: Primary abstract Cucurbitacin B potently suppresses non-small-cell lung cancer growth: identification of intracellular thiols as critical targets. · 2013 · https://pubmed.ncbi.nlm.nih.gov/23340170/ · DOI 10.1016/j.canlet.2013.01.008
Complete structured claim and evidenceAdding N-acetylcysteine attenuated the reported cucurbitacin B cellular effects in the human NSCLC study.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Human NSCLC experiments plus separate cell-free interaction assays.
- limitations
- Compound trapping and redox effects are not distinguished by rescue alone.
- nutrient_topic
- Cucurbitacins collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Cucurbitacins
- plain_language
- Thiol availability changed the experimental response.
- primary_references
- Cucurbitacin B potently suppresses non-small-cell lung cancer growth: identification of intracellular thiols as critical targets. · 2013 · https://pubmed.ncbi.nlm.nih.gov/23340170/ · DOI 10.1016/j.canlet.2013.01.008
Cucurbitacins: thiol chemistry, cytoskeleton, metabolic dependencies and signaling (2026-09-20) · lines 148–154
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human NSCLC experiments plus separate cell-free interaction assays. · source_derived_draft · unverified_draft
## cucurbitacin-b-nac-rescue Thiol availability changed the experimental response. Adding N-acetylcysteine attenuated the reported cucurbitacin B cellular effects in the human NSCLC study. Model: Human NSCLC experiments plus separate cell-free interaction assays. Limitations: Compound trapping and redox effects are not distinguished by rescue alone. Evidence access: Primary abstract Cucurbitacin B potently suppresses non-small-cell lung cancer growth: identification of intracellular thiols as critical targets. · 2013 · https://pubmed.ncbi.nlm.nih.gov/23340170/ · DOI 10.1016/j.canlet.2013.01.008
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.