Component
Human dipeptidyl peptidase 4 / DPP4 / CD26
Human dipeptidyl peptidase 4 / DPP4 / CD26
3 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
Apigenin increased cell-surface CD26/DPP4 expression in HT-29 cells.
Experimental context and source evidence
- evidence_access
- Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
- experimental_contrast
- {"intervention": "Apigenin", "comparator": "Vehicle", "endpoint": "Apigenin increased cell-surface CD26/DPP4 expression in HT-29 cells.", "effect_direction": "increase", "combination": "single", "conditions": []} Explicit extracted experimental comparison; recorded from source.
- experimental_model
- Human colorectal cancer cell line; 30–60 micromolar, 48 hours.
- interpretation_status
- Recorded from source with stated access limits; ungraded, not independent replication.
- limitations
- Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.
- nutrient_topic
- Apigenin collection; exact intervention and molecular form govern interpretation. · Apigenin
- plain_language
- Apigenin increased cell-surface CD26/DPP4 expression in HT-29 cells.
- primary_references
- Apigenin directly interacts with and inhibits topoisomerase 1 to upregulate CD26/DPP4 on colorectal carcinoma cells. | https://pubmed.ncbi.nlm.nih.gov/36618939/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC9815539/ | https://doi.org/10.3389/fphar.2022.1086894
- source_locator
- Reviewed reference api-cd26; Surface expression is not necessarily catalytic activity, glucose control or an anti-tumor endpoint.
Apigenin: detailed mechanisms of action (reviewed 10 October 2026) · lines 724–730
AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed. · supports · Human colorectal cancer cell line; 30–60 micromolar, 48 hours. · Recorded from source · Recorded from source
### api-cd26 Apigenin increased cell-surface CD26/DPP4 expression in HT-29 cells. Surface expression is not necessarily catalytic activity, glucose control or an anti-tumor endpoint. Model and exposure: Human colorectal cancer cell line; 30–60 micromolar, 48 hours. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: Apigenin directly interacts with and inhibits topoisomerase 1 to upregulate CD26/DPP4 on colorectal carcinoma cells. | 2022 | https://pubmed.ncbi.nlm.nih.gov/36618939/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC9815539/ | https://doi.org/10.3389/fphar.2022.1086894 | Access: Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
Complete structured claim and evidenceApigenin plus irinotecan increased CD26 expression in the reported HT-29 combination assay.
Experimental context and source evidence
- evidence_access
- Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
- experimental_condition
- Single-agent comparison reported by the study co-administered · Irinotecan Condition belongs to the full experimental contrast; do not separate a joint intervention.
- experimental_condition
- Single-agent comparison reported by the study Apigenin plus irinotecan · Apigenin Condition belongs to the full experimental contrast; do not separate a joint intervention.
- experimental_contrast
- {"intervention": "Apigenin plus irinotecan", "comparator": "Single-agent comparison reported by the study", "endpoint": "Apigenin plus irinotecan increased CD26 expression in the reported HT-29 combination assay.", "effect_direction": "increase", "combination": "joint", "conditions": [{"entity_slug": "apigenin", "state": "Apigenin plus irinotecan"}, {"entity_slug": "irinotecan", "state": "co-administered"}]} Explicit extracted experimental comparison; recorded from source.
- experimental_model
- Cell-surface CD26 endpoint; the paper also tested other topoisomerase drugs.
- interpretation_status
- Recorded from source with stated access limits; ungraded, not independent replication.
- limitations
- Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.
- nutrient_topic
- Apigenin collection; exact intervention and molecular form govern interpretation. · Apigenin
- plain_language
- Apigenin plus irinotecan increased CD26 expression in the reported HT-29 combination assay.
- primary_references
- Apigenin directly interacts with and inhibits topoisomerase 1 to upregulate CD26/DPP4 on colorectal carcinoma cells. | https://pubmed.ncbi.nlm.nih.gov/36618939/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC9815539/ | https://doi.org/10.3389/fphar.2022.1086894
- source_locator
- Reviewed reference api-irinotecan-cd26; Do not translate this expression interaction into proven synergistic tumor killing or a clinical co-treatment recommendation.
Apigenin: detailed mechanisms of action (reviewed 10 October 2026) · lines 740–746
AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed. · supports · Cell-surface CD26 endpoint; the paper also tested other topoisomerase drugs. · Recorded from source · Recorded from source
### api-irinotecan-cd26 Apigenin plus irinotecan increased CD26 expression in the reported HT-29 combination assay. Do not translate this expression interaction into proven synergistic tumor killing or a clinical co-treatment recommendation. Model and exposure: Cell-surface CD26 endpoint; the paper also tested other topoisomerase drugs. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: Apigenin directly interacts with and inhibits topoisomerase 1 to upregulate CD26/DPP4 on colorectal carcinoma cells. | 2022 | https://pubmed.ncbi.nlm.nih.gov/36618939/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC9815539/ | https://doi.org/10.3389/fphar.2022.1086894 | Access: Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
Complete structured claim and evidenceTOP1 knockdown raised basal CD26 expression and occluded the additional CD26 response to apigenin.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence_access
- Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
- experimental_condition
- TOP1-knockdown cells without apigenin siRNA knockdown · Human DNA topoisomerase I / TOP1 Condition belongs to the full experimental contrast; do not separate a joint intervention.
- experimental_condition
- TOP1-knockdown cells without apigenin Apigenin after TOP1 knockdown · Apigenin Condition belongs to the full experimental contrast; do not separate a joint intervention.
- experimental_contrast
- {"intervention": "Apigenin after TOP1 knockdown", "comparator": "TOP1-knockdown cells without apigenin", "endpoint": "TOP1 knockdown raised basal CD26 expression and occluded the additional CD26 response to apigenin.", "effect_direction": "no_detected_change", "combination": "joint", "conditions": [{"entity_slug": "apigenin", "state": "Apigenin after TOP1 knockdown"}, {"entity_slug": "human-top1", "state": "siRNA knockdown"}]} Explicit extracted experimental comparison; recorded from source.
- experimental_model
- HT-29 cells; over 75% TOP1 knockdown.
- interpretation_status
- Recorded from source with stated access limits; ungraded, not independent replication.
- limitations
- Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.
- nutrient_topic
- Apigenin collection; exact intervention and molecular form govern interpretation. · Apigenin
- plain_language
- TOP1 knockdown raised basal CD26 expression and occluded the additional CD26 response to apigenin.
- primary_references
- Apigenin directly interacts with and inhibits topoisomerase 1 to upregulate CD26/DPP4 on colorectal carcinoma cells. | https://pubmed.ncbi.nlm.nih.gov/36618939/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC9815539/ | https://doi.org/10.3389/fphar.2022.1086894
- source_locator
- Reviewed reference api-top1-knockdown; Supports pathway involvement for this expression endpoint without identifying a clinical therapeutic interaction.
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Apigenin: detailed mechanisms of action (reviewed 10 October 2026) · lines 732–738
AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed. · supports · HT-29 cells; over 75% TOP1 knockdown. · Recorded from source · Recorded from source
### api-top1-knockdown TOP1 knockdown raised basal CD26 expression and occluded the additional CD26 response to apigenin. Supports pathway involvement for this expression endpoint without identifying a clinical therapeutic interaction. Model and exposure: HT-29 cells; over 75% TOP1 knockdown. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: Apigenin directly interacts with and inhibits topoisomerase 1 to upregulate CD26/DPP4 on colorectal carcinoma cells. | 2022 | https://pubmed.ncbi.nlm.nih.gov/36618939/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC9815539/ | https://doi.org/10.3389/fphar.2022.1086894 | Access: Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
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.