Component

Early lung colonization in SLC25A39-dependent breast-cancer models

Early lung colonization in SLC25A39-dependent breast-cancer models. Species, exposure and limitations are retained in each linked claim.

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. DELE1 overexpression largely restored lung colonization by SLC25A39-knockout MDA-MB-231 cells.

    DELE1 overexpression in human breast-cancer cells → Early lung colonization in SLC25A39-dependent breast-cancer models source_derived_draftungraded
    Experimental context and source evidence
    access_level
    selected_indexed_full_text_passages
    evidence_cache
    artifacts/discovery-research/round2-sources/primary-mechanism-passages.json; SHA256 81c0207494f0b2a22fd0af0d70528a5114dfd74367dd99f967f4ada68c53e8c3
    experimental_model
    Human cells injected into mice; 5 mice/group
    exposure
    500,000 injected cells; timing unresolved
    limitations
    Selected indexed primary full-text passages reviewed; supplements not independently inspected in this round. These records do not demonstrate iron-chelation rescue of SLC25A39 loss, clinical benefit, or transfer to pulmonary endothelium.
    organism
    Human cultured cells; mouse xenograft host only for colonization endpoint
    plain_language
    DELE1 overexpression largely restored lung colonization by SLC25A39-knockout MDA-MB-231 cells.
    primary_locator
    https://pmc.ncbi.nlm.nih.gov/articles/PMC12396134/ Figure 4D
    primary_references
    https://doi.org/10.1158/2159-8290.CD-24-1556

    DELE1 bridge: iron sensing and mitochondrial-glutathione-dependent stress signaling · lines 19–28

    Targeted primary-literature curation; selected indexed full-text passages, 2026-09-20. · supports · Human cells injected into mice; 5 mice/group · source_derived_draft · unverified_draft

    DELE1 overexpression largely restored lung colonization by SLC25A39-knockout MDA-MB-231 cells. primary_references: https://doi.org/10.1158/2159-8290.CD-24-1556 primary_locator: https://pmc.ncbi.nlm.nih.gov/articles/PMC12396134/ Figure 4D evidence_cache: artifacts/discovery-research/round2-sources/primary-mechanism-passages.json; SHA256 81c0207494f0b2a22fd0af0d70528a5114dfd74367dd99f967f4ada68c53e8c3 access_level: selected_indexed_full_text_passages experimental_model: Human cells injected into mice; 5 mice/group organism: Human cultured cells; mouse xenograft host only for colonization endpoint exposure: 500,000 injected cells; timing unresolved limitations: Selected indexed primary full-text passages reviewed; supplements not independently inspected in this round. These records do not demonstrate iron-chelation rescue of SLC25A39 loss, clinical benefit, or transfer to pulmonary endothelium. plain_language: DELE1 overexpression largely restored lung colonization by SLC25A39-knockout MDA-MB-231 cells.
    Complete structured claim and evidence

  2. ATF4 activation restored metastatic potential in A39-deficient experimental cells.

    Human activating transcription factor 4 / ATF4 → Early lung colonization in SLC25A39-dependent breast-cancer models source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/glutathione-research/40736010.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "6c5baf25f027a65c991f7d45f87238cad1e474e7e910dceb32aa78a108e6d29e", "start_char": 0, "end_char": 1513, "text_sha256": "6c5baf25f027a65c991f7d45f87238cad1e474e7e910dceb32aa78a108e6d29e"}
    experimental_model
    Genetic screens, cancer models and patient-derived xenografts
    exposure
    SLC25A39 loss and ATF4 CRISPR activation
    limitations
    Cancer-specific mechanism; no inference that dietary or supplemental GSH causes metastasis in people.
    nutrient_topic
    Glutathione research collection; topical membership is not evidence of a direct dietary effect. · GSH
    organism
    Experimental breast-cancer cells and mouse xenografts
    plain_language
    A stress-response pathway provided a bypass in these models.
    primary_references
    [glutathione-p40736010] Mitochondrial Glutathione Import Enables Breast Cancer Metastasis via Integrated Stress Response Signaling. (2025). https://pubmed.ncbi.nlm.nih.gov/40736010/ DOI: 10.1158/2159-8290.cd-24-1556
    tissue_or_cell_type
    Early lung metastatic colonization

    Glutathione: metabolism, signaling and nutrient connections (2026-09-17) · lines 1347–1358

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Genetic screens, cancer models and patient-derived xenografts · source_derived_draft · unverified_draft

    ### glutathione-atf4-metastasis-rescue ATF4 activation restored metastatic potential in A39-deficient experimental cells. Condition category: normal nutrient_topic: Glutathione research collection; topical membership is not evidence of a direct dietary effect. plain_language: A stress-response pathway provided a bypass in these models. organism: Experimental breast-cancer cells and mouse xenografts tissue_or_cell_type: Early lung metastatic colonization experimental_model: Genetic screens, cancer models and patient-derived xenografts limitations: Cancer-specific mechanism; no inference that dietary or supplemental GSH causes metastasis in people. exposure: SLC25A39 loss and ATF4 CRISPR activation evidence_span: {"source_cache": "artifacts/glutathione-research/40736010.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "6c5baf25f027a65c991f7d45f87238cad1e474e7e910dceb32aa78a108e6d29e", "start_char": 0, "end_char": 1513, "text_sha256": "6c5baf25f027a65c991f7d45f87238cad1e474e7e910dceb32aa78a108e6d29e"} [glutathione-p40736010] Mitochondrial Glutathione Import Enables Breast Cancer Metastasis via Integrated Stress Response Signaling. (2025). https://pubmed.ncbi.nlm.nih.gov/40736010/ DOI: 10.1158/2159-8290.cd-24-1556
    Complete structured claim and evidence

  3. A39 loss impaired early metastatic colonization in the tested breast-cancer models.

    SLC25A39-knockout mammalian cells → Early lung colonization in SLC25A39-dependent breast-cancer models source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/glutathione-research/40736010.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "6c5baf25f027a65c991f7d45f87238cad1e474e7e910dceb32aa78a108e6d29e", "start_char": 0, "end_char": 1513, "text_sha256": "6c5baf25f027a65c991f7d45f87238cad1e474e7e910dceb32aa78a108e6d29e"}
    experimental_model
    Genetic screens, cancer models and patient-derived xenografts
    exposure
    SLC25A39 loss and ATF4 CRISPR activation
    limitations
    Cancer-specific mechanism; no inference that dietary or supplemental GSH causes metastasis in people.
    nutrient_topic
    Glutathione research collection; topical membership is not evidence of a direct dietary effect. · GSH
    organism
    Experimental breast-cancer cells and mouse xenografts
    plain_language
    Glutathione-dependent machinery can also support an unwanted cell process.
    primary_references
    [glutathione-p40736010] Mitochondrial Glutathione Import Enables Breast Cancer Metastasis via Integrated Stress Response Signaling. (2025). https://pubmed.ncbi.nlm.nih.gov/40736010/ DOI: 10.1158/2159-8290.cd-24-1556
    tissue_or_cell_type
    Early lung metastatic colonization

    Glutathione: metabolism, signaling and nutrient connections (2026-09-17) · lines 1321–1332

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Genetic screens, cancer models and patient-derived xenografts · source_derived_draft · unverified_draft

    ### glutathione-metastasis-a39 A39 loss impaired early metastatic colonization in the tested breast-cancer models. Condition category: normal nutrient_topic: Glutathione research collection; topical membership is not evidence of a direct dietary effect. plain_language: Glutathione-dependent machinery can also support an unwanted cell process. organism: Experimental breast-cancer cells and mouse xenografts tissue_or_cell_type: Early lung metastatic colonization experimental_model: Genetic screens, cancer models and patient-derived xenografts limitations: Cancer-specific mechanism; no inference that dietary or supplemental GSH causes metastasis in people. exposure: SLC25A39 loss and ATF4 CRISPR activation evidence_span: {"source_cache": "artifacts/glutathione-research/40736010.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "6c5baf25f027a65c991f7d45f87238cad1e474e7e910dceb32aa78a108e6d29e", "start_char": 0, "end_char": 1513, "text_sha256": "6c5baf25f027a65c991f7d45f87238cad1e474e7e910dceb32aa78a108e6d29e"} [glutathione-p40736010] Mitochondrial Glutathione Import Enables Breast Cancer Metastasis via Integrated Stress Response Signaling. (2025). https://pubmed.ncbi.nlm.nih.gov/40736010/ DOI: 10.1158/2159-8290.cd-24-1556
    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