Component

Whole-cell phosphorylated STAT3 abundance in human cells

3 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. SFX-01 reduced phosphorylated STAT3 relative to antiestrogen-only treatments in BB3RC61 cells.

    SFX-01, sulforaphane stabilized in an alpha-cyclodextrin complex → Whole-cell phosphorylated STAT3 abundance in human cells source_derived_draftungraded
    Experimental context and source evidence
    experimental_model
    Human antiestrogen-resistant metastatic breast cancer sample BB3RC61
    exposure
    72-hour treatment. Supplementary reagent protocol uses 5 micromolar SFX-01, 1 micromolar 4-OH-tamoxifen or 0.1 micromolar fulvestrant; these concentrations are explicitly stated for cell lines, and patient-specific dosing is not independently confirmed here.
    limitations
    The chemical probe and stabilized formulation are separate experimental actors. Capture supports engagement but does not identify the modified STAT3 cysteine or demonstrate that APT2 mediates the effect. No GPX4 time-course endpoint. Primary cell/PDX studies are not evidence of benefit from dietary broccoli.
    organism
    Human
    primary_locator
    Figure 4d; Results: SFX-01 targets STAT3 signaling.
    primary_references
    https://doi.org/10.1038/s41388-020-1335-z

    APT2-STAT3 cycling and a competing sulforaphane target route · lines 96–102

    Selected primary observations: 10.1038/s41586-020-2799-2 and 10.1038/s41388-020-1335-z. · supports · Human antiestrogen-resistant metastatic breast cancer sample BB3RC61 · source_derived_draft · unverified_draft

    SFX-01 reduced phosphorylated STAT3 relative to antiestrogen-only treatments in BB3RC61 cells. primary_references: https://doi.org/10.1038/s41388-020-1335-z primary_locator: Figure 4d; Results: SFX-01 targets STAT3 signaling. organism: Human experimental_model: Human antiestrogen-resistant metastatic breast cancer sample BB3RC61 exposure: 72-hour treatment. Supplementary reagent protocol uses 5 micromolar SFX-01, 1 micromolar 4-OH-tamoxifen or 0.1 micromolar fulvestrant; these concentrations are explicitly stated for cell lines, and patient-specific dosing is not independently confirmed here. limitations: The chemical probe and stabilized formulation are separate experimental actors. Capture supports engagement but does not identify the modified STAT3 cysteine or demonstrate that APT2 mediates the effect. No GPX4 time-course endpoint. Primary cell/PDX studies are not evidence of benefit from dietary broccoli.
    Complete structured claim and evidence

  2. SFX-01 did not repress STAT3 activity in the reported previously SFX-01-treated, resistant BB7121 sample.

    SFX-01, sulforaphane stabilized in an alpha-cyclodextrin complex → Whole-cell phosphorylated STAT3 abundance in human cells source_derived_draftungraded
    Experimental context and source evidence
    experimental_model
    Human metastatic breast cancer patient-derived sample BB7121
    exposure
    Prior clinical SFX-01 exposure with progression; ex vivo STAT3 assay. Exact panel exposure unresolved.
    limitations
    The chemical probe and stabilized formulation are separate experimental actors. Capture supports engagement but does not identify the modified STAT3 cysteine or demonstrate that APT2 mediates the effect. No GPX4 time-course endpoint. Primary cell/PDX studies are not evidence of benefit from dietary broccoli. A single resistant sample does not determine the mechanism of resistance. Supplementary legend/main-text result reviewed; raw image not quantitatively reanalyzed.
    organism
    Human
    primary_locator
    Results: SFX-01 targets STAT3 signaling; Supplementary Figure S4c.
    primary_references
    https://doi.org/10.1038/s41388-020-1335-z

    APT2-STAT3 cycling and a competing sulforaphane target route · lines 105–111

    Selected primary observations: 10.1038/s41586-020-2799-2 and 10.1038/s41388-020-1335-z. · supports · Human metastatic breast cancer patient-derived sample BB7121 · source_derived_draft · unverified_draft

    SFX-01 did not repress STAT3 activity in the reported previously SFX-01-treated, resistant BB7121 sample. primary_references: https://doi.org/10.1038/s41388-020-1335-z primary_locator: Results: SFX-01 targets STAT3 signaling; Supplementary Figure S4c. organism: Human experimental_model: Human metastatic breast cancer patient-derived sample BB7121 exposure: Prior clinical SFX-01 exposure with progression; ex vivo STAT3 assay. Exact panel exposure unresolved. limitations: The chemical probe and stabilized formulation are separate experimental actors. Capture supports engagement but does not identify the modified STAT3 cysteine or demonstrate that APT2 mediates the effect. No GPX4 time-course endpoint. Primary cell/PDX studies are not evidence of benefit from dietary broccoli. A single resistant sample does not determine the mechanism of resistance. Supplementary legend/main-text result reviewed; raw image not quantitatively reanalyzed.
    Complete structured claim and evidence

  3. Solasonine did not change whole-cell phosphorylated STAT3 in the reported immunoblots.

    Solasonine → Whole-cell phosphorylated STAT3 abundance in human cells source_derived_draftungraded
    Experimental context and source evidence
    experimental_model
    Human NOZ and GBC-SD gallbladder cancer cells
    exposure
    Methods 2.2 describes 48-hour cellular drug treatments with refresh at 24 hours; exact concentration must be checked per figure and is not inferred from another assay.
    limitations
    Human cancer-cell experiments; no clinical or dietary inference. Solasonine exposure is not equivalent to APT2 depletion, ML349, or sulforaphane. Mutant rescue does not by itself establish selectivity or normal baseline mutant function. Figure 5C calls this APT2 activity, but Methods 2.17 describes an anti-LYPLA2 ELISA with mass-concentration standards and an HRP/TMB readout from cell supernatants. No direct APT2 substrate-turnover assay is described there. The result is retained as an author-labelled activity proxy, not established catalytic inhibition. This methodological qualification does not invalidate the separately reported binding or cellular observations.
    organism
    Human
    primary_locator
    Figure 4A; Results 3.4.
    primary_references
    https://doi.org/10.1002/ptr.70245

    APT2, STAT3 and GPX4: opposing branches and assay qualification · lines 87–93

    Primary observations: 10.1038/s41467-025-56344-5 and 10.1002/ptr.70245; selected full-text review 2026-09-20. · supports · Human NOZ and GBC-SD gallbladder cancer cells · source_derived_draft · unverified_draft

    Solasonine did not change whole-cell phosphorylated STAT3 in the reported immunoblots. primary_references: https://doi.org/10.1002/ptr.70245 primary_locator: Figure 4A; Results 3.4. organism: Human experimental_model: Human NOZ and GBC-SD gallbladder cancer cells exposure: Methods 2.2 describes 48-hour cellular drug treatments with refresh at 24 hours; exact concentration must be checked per figure and is not inferred from another assay. limitations: Human cancer-cell experiments; no clinical or dietary inference. Solasonine exposure is not equivalent to APT2 depletion, ML349, or sulforaphane. Mutant rescue does not by itself establish selectivity or normal baseline mutant function. Figure 5C calls this APT2 activity, but Methods 2.17 describes an anti-LYPLA2 ELISA with mass-concentration standards and an HRP/TMB readout from cell supernatants. No direct APT2 substrate-turnover assay is described there. The result is retained as an author-labelled activity proxy, not established catalytic inhibition. This methodological qualification does not invalidate the separately reported binding or cellular observations.
    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.

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