Component
Human CDKN2A p16INK4a isoform
Experimental species, exposure and limitations are retained on each linked 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
Indicaxanthin treatment reactivated p16INK4a mRNA and increased its protein in Caco-2 cells.
Experimental context and source evidence
- dose
- Purified indicaxanthin; growth IC50 115 +/- 15 micromolar, exact exposure series not in accessed abstract
- duration
- Exposure duration not specified in the accessed primary abstract
- evidence_access
- Primary PubMed abstract.
- evidence_scope
- literature_reviewed; model-specific source-derived curation
- experimental_model
- Proliferating human Caco-2 colorectal cancer cells
- limitations
- Locus-specific demethylation does not imply universal DNA demethylation. A cell-line response is not cancer prevention in people.
- nutrient_topic
- Dedicated indicaxanthin chapter; original betalain family identity and shared claims preserved. · Indicaxanthin
- organism
- Proliferating human Caco-2 colorectal cancer cells
- plain_language
- Indicaxanthin treatment reactivated p16INK4a mRNA and increased its protein in Caco-2 cells.
- primary_references
- Anti-proliferative and pro-apoptotic activity of whole extract and isolated indicaxanthin from Opuntia ficus-indica associated with re-activation of the onco-suppressor p16(INK4a) gene in human colorectal carcinoma (Caco-2) cells. (2014). https://pubmed.ncbi.nlm.nih.gov/24937448/ DOI: 10.1016/j.bbrc.2014.06.029
- route
- In vitro addition
- tissue
- Epigenetic and growth assays
Indicaxanthin: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 393–402
Original AI-assisted curation of thirteen additional primary studies, with twenty-six existing claims from eight studies linked unchanged. Study-specific citations and limitations retained. Not publisher full text. · supports · Proliferating human Caco-2 colorectal cancer cells · source_derived_draft · unverified_draft
## indicaxanthin-p16-expression Indicaxanthin treatment reactivated p16INK4a mRNA and increased its protein in Caco-2 cells. Model/species: Proliferating human Caco-2 colorectal cancer cells Tissue: Epigenetic and growth assays Exposure: Purified indicaxanthin; growth IC50 115 +/- 15 micromolar, exact exposure series not in accessed abstract Route: In vitro addition Duration: Exposure duration not specified in the accessed primary abstract Limits: Locus-specific demethylation does not imply universal DNA demethylation. A cell-line response is not cancer prevention in people. Primary reference: Anti-proliferative and pro-apoptotic activity of whole extract and isolated indicaxanthin from Opuntia ficus-indica associated with re-activation of the onco-suppressor p16(INK4a) gene in human colorectal carcinoma (Caco-2) cells. (2014). https://pubmed.ncbi.nlm.nih.gov/24937448/ DOI: 10.1016/j.bbrc.2014.06.029 Access: Primary PubMed abstract.
Complete structured claim and evidence
Where it participates (unsigned role)
Indicaxanthin treatment demethylated the p16INK4a promoter in proliferating Caco-2 cells.
Experimental context and source evidence
- dose
- Purified indicaxanthin; growth IC50 115 +/- 15 micromolar, exact exposure series not in accessed abstract
- duration
- Exposure duration not specified in the accessed primary abstract
- evidence_access
- Primary PubMed abstract.
- evidence_scope
- literature_reviewed; model-specific source-derived curation
- experimental_model
- Proliferating human Caco-2 colorectal cancer cells
- limitations
- Locus-specific demethylation does not imply universal DNA demethylation. A cell-line response is not cancer prevention in people.
- nutrient_topic
- Dedicated indicaxanthin chapter; original betalain family identity and shared claims preserved. · Indicaxanthin
- organism
- Proliferating human Caco-2 colorectal cancer cells
- plain_language
- Indicaxanthin treatment demethylated the p16INK4a promoter in proliferating Caco-2 cells.
- primary_references
- Anti-proliferative and pro-apoptotic activity of whole extract and isolated indicaxanthin from Opuntia ficus-indica associated with re-activation of the onco-suppressor p16(INK4a) gene in human colorectal carcinoma (Caco-2) cells. (2014). https://pubmed.ncbi.nlm.nih.gov/24937448/ DOI: 10.1016/j.bbrc.2014.06.029
- route
- In vitro addition
- tissue
- Epigenetic and growth assays
Indicaxanthin: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 382–391
Original AI-assisted curation of thirteen additional primary studies, with twenty-six existing claims from eight studies linked unchanged. Study-specific citations and limitations retained. Not publisher full text. · supports · Proliferating human Caco-2 colorectal cancer cells · source_derived_draft · unverified_draft
## indicaxanthin-p16-promoter Indicaxanthin treatment demethylated the p16INK4a promoter in proliferating Caco-2 cells. Model/species: Proliferating human Caco-2 colorectal cancer cells Tissue: Epigenetic and growth assays Exposure: Purified indicaxanthin; growth IC50 115 +/- 15 micromolar, exact exposure series not in accessed abstract Route: In vitro addition Duration: Exposure duration not specified in the accessed primary abstract Limits: Locus-specific demethylation does not imply universal DNA demethylation. A cell-line response is not cancer prevention in people. Primary reference: Anti-proliferative and pro-apoptotic activity of whole extract and isolated indicaxanthin from Opuntia ficus-indica associated with re-activation of the onco-suppressor p16(INK4a) gene in human colorectal carcinoma (Caco-2) cells. (2014). https://pubmed.ncbi.nlm.nih.gov/24937448/ DOI: 10.1016/j.bbrc.2014.06.029 Access: Primary PubMed abstract.
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.