Component

Human beta-catenin / CTNNB1

Context-specific entity; species, compartment and exposure are stated on each claim.

5 recorded relationships. Experimental role, claim status and evidence remain attached to each record.

Read recorded mechanisms Open recursive mind map

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.

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.

Recorded relationships

What acts on it

  1. An Akt-dependent signaling cascade through CaSR promoted beta-catenin nuclear translocation in strontium-treated primary human osteoblasts.

    Strontium ion / Sr2+ → Human beta-catenin / CTNNB1 source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Human primary osteoblast signaling experiments.
    limitations
    Does not prove direct binding to Akt or beta-catenin; Akt isoform not resolved here.
    nutrient_topic
    Strontium collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Strontium
    plain_language
    A receptor signal can reach a transcriptional regulator through Akt.
    primary_references
    An Akt-dependent increase in canonical Wnt signaling and a decrease in sclerostin protein levels are involved in strontium ranelate-induced osteogenic effects in human osteoblasts. · 2011 · https://pubmed.ncbi.nlm.nih.gov/21566129/ · DOI 10.1074/jbc.M111.251116

    Strontium: calcium interactions, cellular mechanisms and mineralization (2026-09-19) · lines 182–188

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human primary osteoblast signaling experiments. · source_derived_draft · unverified_draft

    ## strontium-human-beta-catenin A receptor signal can reach a transcriptional regulator through Akt. An Akt-dependent signaling cascade through CaSR promoted beta-catenin nuclear translocation in strontium-treated primary human osteoblasts. Model: Human primary osteoblast signaling experiments. Limitations: Does not prove direct binding to Akt or beta-catenin; Akt isoform not resolved here. Evidence access: Primary abstract An Akt-dependent increase in canonical Wnt signaling and a decrease in sclerostin protein levels are involved in strontium ranelate-induced osteogenic effects in human osteoblasts. · 2011 · https://pubmed.ncbi.nlm.nih.gov/21566129/ · DOI 10.1074/jbc.M111.251116
    Complete structured claim and evidence

  2. LiCl inhibited GSK3beta and stabilized free beta-catenin in cultured human thyrocytes.

    Lithium ion (Li+) → Human beta-catenin / CTNNB1 source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Primary and neoplastic human-cell preparations; dose-response assays.
    limitations
    Historical cell-line identities and experimental conditions limit extrapolation.
    nutrient_topic
    Lithium collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Lithium
    plain_language
    Thyroid growth signaling can change independently of hormone release.
    primary_references
    Lithium stimulates proliferation in cultured thyrocytes by activating Wnt/beta-catenin signalling. · 2005 · https://pubmed.ncbi.nlm.nih.gov/16322400/ · DOI 10.1530/eje.1.02038

    Lithium: metal-sensitive enzymes, transport and cross-nutrient mechanisms (2026-09-19) · lines 408–414

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Primary and neoplastic human-cell preparations; dose-response assays. · source_derived_draft · unverified_draft

    ## lithium-thyroid-beta-catenin Thyroid growth signaling can change independently of hormone release. LiCl inhibited GSK3beta and stabilized free beta-catenin in cultured human thyrocytes. Model: Primary and neoplastic human-cell preparations; dose-response assays. Limitations: Historical cell-line identities and experimental conditions limit extrapolation. Evidence access: Primary abstract Lithium stimulates proliferation in cultured thyrocytes by activating Wnt/beta-catenin signalling. · 2005 · https://pubmed.ncbi.nlm.nih.gov/16322400/ · DOI 10.1530/eje.1.02038
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. Strontium increased mineralization in primary human osteoblast cultures in the 2011 study.

    Strontium ion / Sr2+ → Mineralization in strontium-treated human osteoblast cultures source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Primary human osteoblast mineralization assay.
    limitations
    Later rat primary-culture work directly challenged a general mineralization-promoting interpretation; matched exposure and culture comparisons remain necessary.
    nutrient_topic
    Strontium collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Strontium
    plain_language
    This study found more mineral deposition in its culture system.
    primary_references
    An Akt-dependent increase in canonical Wnt signaling and a decrease in sclerostin protein levels are involved in strontium ranelate-induced osteogenic effects in human osteoblasts. · 2011 · https://pubmed.ncbi.nlm.nih.gov/21566129/ · DOI 10.1074/jbc.M111.251116

    Strontium: calcium interactions, cellular mechanisms and mineralization (2026-09-19) · lines 190–196

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Primary human osteoblast mineralization assay. · source_derived_draft · unverified_draft

    ## strontium-human-mineralization-positive This study found more mineral deposition in its culture system. Strontium increased mineralization in primary human osteoblast cultures in the 2011 study. Model: Primary human osteoblast mineralization assay. Limitations: Later rat primary-culture work directly challenged a general mineralization-promoting interpretation; matched exposure and culture comparisons remain necessary. Evidence access: Primary abstract An Akt-dependent increase in canonical Wnt signaling and a decrease in sclerostin protein levels are involved in strontium ranelate-induced osteogenic effects in human osteoblasts. · 2011 · https://pubmed.ncbi.nlm.nih.gov/21566129/ · DOI 10.1074/jbc.M111.251116
    Complete structured claim and evidence

  2. At 5 mM LiCl, thyrocyte proliferation increased; dominant-negative TCF4 reduced this response by about half.

    Lithium ion (Li+) → Human cultured-thyrocyte proliferation source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Human cultured thyrocytes; TCF4 versus CREB pathway perturbation.
    limitations
    High cell-culture exposure; not a quantified human goiter or cancer risk.
    nutrient_topic
    Lithium collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Lithium
    plain_language
    Blocking a downstream regulator weakened the growth response.
    primary_references
    Lithium stimulates proliferation in cultured thyrocytes by activating Wnt/beta-catenin signalling. · 2005 · https://pubmed.ncbi.nlm.nih.gov/16322400/ · DOI 10.1530/eje.1.02038

    Lithium: metal-sensitive enzymes, transport and cross-nutrient mechanisms (2026-09-19) · lines 416–422

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human cultured thyrocytes; TCF4 versus CREB pathway perturbation. · source_derived_draft · unverified_draft

    ## lithium-thyroid-wnt-growth Blocking a downstream regulator weakened the growth response. At 5 mM LiCl, thyrocyte proliferation increased; dominant-negative TCF4 reduced this response by about half. Model: Human cultured thyrocytes; TCF4 versus CREB pathway perturbation. Limitations: High cell-culture exposure; not a quantified human goiter or cancer risk. Evidence access: Primary abstract Lithium stimulates proliferation in cultured thyrocytes by activating Wnt/beta-catenin signalling. · 2005 · https://pubmed.ncbi.nlm.nih.gov/16322400/ · DOI 10.1530/eje.1.02038
    Complete structured claim and evidence

  3. 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.

    Dihydrocapsaicin → Proliferation and metastasis of melanoma cells source_derived_draftungraded
    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

    Dihydrocapsaicin: the second capsaicinoid, the hypothermia it is used to induce, what the gut and liver do to it, and what it does without TRPV1 (2026-09-21) · lines 738–749

    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

In the sources

Preserved passages that mention this component, quoted exactly. Open one to read it in context.

    This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.

    Evidence, AI assistance and curation standards