Component
Proliferation and metastasis of melanoma cells
Proliferation and metastasis of melanoma cells. 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.
What acts on it
Melanoma A375 and MV3 cell lines treated with dihydrocapsaicin showed significantly suppressed proliferation, migration and invasion, dihydrocapsaicin inhibited xenograft tumour growth and pulmonary metastasis in a NOD/SCID mouse model, beta-catenin was downregulated after treatment along with cyclin D1, c-Myc, MMP2 and MMP7, and mechanistically dihydrocapsaicin accelerated ubiquitination of beta-catenin and upregulated the E3 ubiquitin protein ligase BTRC.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/dihydrocapsaicin-research/33833997.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5da9019700891a189af0778272381e19a8f276d17d20c59c5f74fbc67b15454e", "start_char": 0, "end_char": 1370, "text_sha256": "5da9019700891a189af0778272381e19a8f276d17d20c59c5f74fbc67b15454e"}
- experimental_model
- Melanoma A375 and MV3 cell lines with a NOD/SCID mouse xenograft and beta-catenin overexpression rescue
- exposure
- Dihydrocapsaicin at 100 micromolar, with exogenous beta-catenin overexpression as the rescue
- limitations
- A corrigendum was published against this article in 2022 stating that four transwell and soft agar images in Figures 5 and 6 were presented with incorrect pictures. Those are the beta-catenin rescue figures, which carry the mechanistic conclusion. The descriptive anti-proliferative result does not rest on them; the mechanism does.
- 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 and mouse
- plain_language
- It slowed melanoma growth and spread, apparently by marking a growth signal for destruction.
- primary_references
- [dhc-p33833997] Dihydrocapsaicin Inhibits Cell Proliferation and Metastasis in Melanoma via Down-regulating β-Catenin Pathway. (2021). https://pubmed.ncbi.nlm.nih.gov/33833997/ DOI: 10.3389/fonc.2021.648052
- tissue_or_cell_type
- Melanoma
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Melanoma A375 and MV3 cell lines with a NOD/SCID mouse xenograft and beta-catenin overexpression rescue · source_derived_draft · unverified_draft
### dhc-melanoma-beta-catenin Melanoma A375 and MV3 cell lines treated with dihydrocapsaicin showed significantly suppressed proliferation, migration and invasion, dihydrocapsaicin inhibited xenograft tumour growth and pulmonary metastasis in a NOD/SCID mouse model, beta-catenin was downregulated after treatment along with cyclin D1, c-Myc, MMP2 and MMP7, and mechanistically dihydrocapsaicin accelerated ubiquitination of beta-catenin and upregulated the E3 ubiquitin protein ligase BTRC. Condition category: normal 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 slowed melanoma growth and spread, apparently by marking a growth signal for destruction. organism: Human cells and mouse tissue_or_cell_type: Melanoma experimental_model: Melanoma A375 and MV3 cell lines with a NOD/SCID mouse xenograft and beta-catenin overexpression rescue limitations: A corrigendum was published against this article in 2022 stating that four transwell and soft agar images in Figures 5 and 6 were presented with incorrect pictures. Those are the beta-catenin rescue figures, which carry the mechanistic conclusion. The descriptive anti-proliferative result does not rest on them; the mechanism does. exposure: Dihydrocapsaicin at 100 micromolar, with exogenous beta-catenin overexpression as the rescue evidence_span: {"source_cache": "artifacts/dihydrocapsaicin-research/33833997.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5da9019700891a189af0778272381e19a8f276d17d20c59c5f74fbc67b15454e", "start_char": 0, "end_char": 1370, "text_sha256": "5da9019700891a189af0778272381e19a8f276d17d20c59c5f74fbc67b15454e"} [dhc-p33833997] Dihydrocapsaicin Inhibits Cell Proliferation and Metastasis in Melanoma via Down-regulating β-Catenin Pathway. (2021). https://pubmed.ncbi.nlm.nih.gov/33833997/ DOI: 10.3389/fonc.2021.648052
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.