Component
S-phase arrest in HepG2 hepatoma cells
Cell cycle distribution after treatment.
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.
What acts on it
Lariciresinol inhibited proliferation of hepatoma cells and induced cell cycle arrest in S phase.
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 HepG2 hepatoma cells
- exposure
- Lariciresinol
- limitations
- No cyclin or cyclin-dependent kinase is identified in the abstract.
- organism
- Human HepG2 hepatoma cells
- plain_language
- Lariciresinol inhibited proliferation of hepatoma cells and induced cell cycle arrest in S phase.
- primary_references
- Proteomic analysis of apoptosis induction by lariciresinol in human HepG2 cells. (2016). https://pubmed.ncbi.nlm.nih.gov/27417256/ DOI: 10.1016/j.cbi.2016.07.013
- route
- In vitro
- tissue
- Cell cycle distribution and proliferation
Lariciresinol: five molecules under one name, and the mechanisms each one carries (2026-09-22) · lines 220–229
Original AI-assisted curation of twelve primary studies, every abstract read and all DOIs cross-checked against live PubMed metadata. Mechanism edges only, with no conclusion or claim of benefit recorded. Three author clusters account for eight of the twelve and carry shared laboratory keys. Study-specific concentrations, negative findings and limitations retained. Not publisher full text. · supports · · source_derived_draft · unverified_draft
## lariciresinol-arrests-hepatoma-cells-in-s-phase Lariciresinol inhibited proliferation of hepatoma cells and induced cell cycle arrest in S phase. Model/species: Human HepG2 hepatoma cells Tissue/system: Cell cycle distribution and proliferation Exposure: Lariciresinol Route: In vitro Duration: Not stated here Limits: No cyclin or cyclin-dependent kinase is identified in the abstract. Primary reference: Proteomic analysis of apoptosis induction by lariciresinol in human HepG2 cells. (2016). https://pubmed.ncbi.nlm.nih.gov/27417256/ DOI: 10.1016/j.cbi.2016.07.013 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.