Component
Epithelial-mesenchymal transition marker expression
Epithelial-mesenchymal transition marker expression. Species, exposure and limitations are retained in each linked claim.
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.
Where it participates (unsigned role)
Dihydrocapsaicin significantly and dose-dependently inhibited the migration and invasion of gastric cancer cells NCI-N87 and HGC-27, significantly increased the expression of TRPV1 and E-cadherin proteins and inhibited the expression of N-cadherin, vimentin and Snail proteins, and functional rescue experiments confirmed that when TRPV1 expression was inhibited the inhibitory effect on migration and invasion was significantly weakened.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence_span
- {"source_cache": "artifacts/dihydrocapsaicin-research/42509404.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "55ec938b5e2c0b1421c473c60c3468ad24770198ee9d1f6549c62af579bf4c4c", "start_char": 0, "end_char": 1925, "text_sha256": "55ec938b5e2c0b1421c473c60c3468ad24770198ee9d1f6549c62af579bf4c4c"}
- experimental_model
- Human gastric cancer cell lines NCI-N87 and HGC-27 with western blotting and TRPV1 knockdown rescue experiments
- exposure
- Dihydrocapsaicin at a range of concentrations, with TRPV1 expression interfered as the test of mediation
- limitations
- The knockdown rescue is the strength here. Note the unusual direction: the compound raised expression of its own receptor rather than merely activating it.
- nutrient_topic
- Dihydrocapsaicin research collection; topical membership is not evidence of a direct clinical effect, and dihydrocapsaicin is recorded separately from capsaicin. · Dihydrocapsaicin
- organism
- Human cells
- plain_language
- It holds gastric cancer cells in place by pushing them back towards a settled, non-migrating state.
- primary_references
- [dhc-p42509404] Dihydrocapsaicin suppresses the migration and invasion of gastric cancer cells by upregulating TRPV1 expression. (2026). https://pubmed.ncbi.nlm.nih.gov/42509404/ DOI: 10.1007/s11626-026-01226-3
- tissue_or_cell_type
- Gastric cancer cells
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human gastric cancer cell lines NCI-N87 and HGC-27 with western blotting and TRPV1 knockdown rescue experiments · source_derived_draft · unverified_draft
### dhc-gastric-cancer-migration Dihydrocapsaicin significantly and dose-dependently inhibited the migration and invasion of gastric cancer cells NCI-N87 and HGC-27, significantly increased the expression of TRPV1 and E-cadherin proteins and inhibited the expression of N-cadherin, vimentin and Snail proteins, and functional rescue experiments confirmed that when TRPV1 expression was inhibited the inhibitory effect on migration and invasion was significantly weakened. Condition category: machinery_impairment nutrient_topic: Dihydrocapsaicin research collection; topical membership is not evidence of a direct clinical effect, and dihydrocapsaicin is recorded separately from capsaicin. plain_language: It holds gastric cancer cells in place by pushing them back towards a settled, non-migrating state. organism: Human cells tissue_or_cell_type: Gastric cancer cells experimental_model: Human gastric cancer cell lines NCI-N87 and HGC-27 with western blotting and TRPV1 knockdown rescue experiments limitations: The knockdown rescue is the strength here. Note the unusual direction: the compound raised expression of its own receptor rather than merely activating it. exposure: Dihydrocapsaicin at a range of concentrations, with TRPV1 expression interfered as the test of mediation evidence_span: {"source_cache": "artifacts/dihydrocapsaicin-research/42509404.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "55ec938b5e2c0b1421c473c60c3468ad24770198ee9d1f6549c62af579bf4c4c", "start_char": 0, "end_char": 1925, "text_sha256": "55ec938b5e2c0b1421c473c60c3468ad24770198ee9d1f6549c62af579bf4c4c"} [dhc-p42509404] Dihydrocapsaicin suppresses the migration and invasion of gastric cancer cells by upregulating TRPV1 expression. (2026). https://pubmed.ncbi.nlm.nih.gov/42509404/ DOI: 10.1007/s11626-026-01226-3
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.