Component

Copper-exposure-induced SLC7A11 expression in human MDA-MB-231 cells

Copper-exposure-induced SLC7A11 expression in human MDA-MB-231 cells. 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.

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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. ATOX1 knockdown also impaired copper-induced SLC7A11 expression.

    Human copper chaperone ATOX1 → Copper-exposure-induced SLC7A11 expression in human MDA-MB-231 cells source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/copper-research/40944334.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "6df1716e8998546d22a1d96116e1bc35b1f7e24c94868ec5e441ada6a2be3e89", "start_char": 0, "end_char": 1634, "text_sha256": "6df1716e8998546d22a1d96116e1bc35b1f7e24c94868ec5e441ada6a2be3e89"}
    experimental_model
    Copper and iron exposure with transcription-factor knockdown
    exposure
    CuCl2 or FeCl2 exposure; NFE2L2 or ATOX1 knockdown
    limitations
    One cancer-cell model. Expression changes do not prove increased glutathione synthesis, tumor progression, or a clinical nutrient interaction.
    nutrient_topic
    Copper research collection; topical membership is not evidence of a direct dietary effect. · Copper
    organism
    Human MDA-MB-231 breast cancer cells
    plain_language
    A copper-handling protein participated in this gene-expression response.
    primary_references
    [copper-p40944334] Copper induces cystine/glutamate antiporter SLC7A11 through the activation of Nrf2 and Atox1 pathways. (2025). https://pubmed.ncbi.nlm.nih.gov/40944334/ DOI: 10.1080/10715762.2025.2560847
    tissue_or_cell_type
    Cellular amino-acid transport machinery

    Copper: transport, cuproenzymes, deficiency, excess and nutrient interactions (2026-09-17) · lines 1313–1324

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Copper and iron exposure with transcription-factor knockdown · source_derived_draft · unverified_draft

    ### copper-atox1-slc7a11 ATOX1 knockdown also impaired copper-induced SLC7A11 expression. Condition category: normal nutrient_topic: Copper research collection; topical membership is not evidence of a direct dietary effect. plain_language: A copper-handling protein participated in this gene-expression response. organism: Human MDA-MB-231 breast cancer cells tissue_or_cell_type: Cellular amino-acid transport machinery experimental_model: Copper and iron exposure with transcription-factor knockdown limitations: One cancer-cell model. Expression changes do not prove increased glutathione synthesis, tumor progression, or a clinical nutrient interaction. exposure: CuCl2 or FeCl2 exposure; NFE2L2 or ATOX1 knockdown evidence_span: {"source_cache": "artifacts/copper-research/40944334.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "6df1716e8998546d22a1d96116e1bc35b1f7e24c94868ec5e441ada6a2be3e89", "start_char": 0, "end_char": 1634, "text_sha256": "6df1716e8998546d22a1d96116e1bc35b1f7e24c94868ec5e441ada6a2be3e89"} [copper-p40944334] Copper induces cystine/glutamate antiporter SLC7A11 through the activation of Nrf2 and Atox1 pathways. (2025). https://pubmed.ncbi.nlm.nih.gov/40944334/ DOI: 10.1080/10715762.2025.2560847
    Complete structured claim and evidence

  2. CuCl2 treatment induced SLC7A11 expression in human MDA-MB-231 cells.

    Copper(II) ion → Copper-exposure-induced SLC7A11 expression in human MDA-MB-231 cells source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/copper-research/40944334.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "6df1716e8998546d22a1d96116e1bc35b1f7e24c94868ec5e441ada6a2be3e89", "start_char": 0, "end_char": 1634, "text_sha256": "6df1716e8998546d22a1d96116e1bc35b1f7e24c94868ec5e441ada6a2be3e89"}
    experimental_model
    Copper and iron exposure with transcription-factor knockdown
    exposure
    CuCl2 or FeCl2 exposure; NFE2L2 or ATOX1 knockdown
    limitations
    One cancer-cell model. Expression changes do not prove increased glutathione synthesis, tumor progression, or a clinical nutrient interaction.
    nutrient_topic
    Copper research collection; topical membership is not evidence of a direct dietary effect. · Copper
    organism
    Human MDA-MB-231 breast cancer cells
    plain_language
    Copper exposure changed part of the cystine-entry system in these cells.
    primary_references
    [copper-p40944334] Copper induces cystine/glutamate antiporter SLC7A11 through the activation of Nrf2 and Atox1 pathways. (2025). https://pubmed.ncbi.nlm.nih.gov/40944334/ DOI: 10.1080/10715762.2025.2560847
    tissue_or_cell_type
    Cellular amino-acid transport machinery

    Copper: transport, cuproenzymes, deficiency, excess and nutrient interactions (2026-09-17) · lines 1274–1285

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Copper and iron exposure with transcription-factor knockdown · source_derived_draft · unverified_draft

    ### copper-cu-slc7a11 CuCl2 treatment induced SLC7A11 expression in human MDA-MB-231 cells. Condition category: normal nutrient_topic: Copper research collection; topical membership is not evidence of a direct dietary effect. plain_language: Copper exposure changed part of the cystine-entry system in these cells. organism: Human MDA-MB-231 breast cancer cells tissue_or_cell_type: Cellular amino-acid transport machinery experimental_model: Copper and iron exposure with transcription-factor knockdown limitations: One cancer-cell model. Expression changes do not prove increased glutathione synthesis, tumor progression, or a clinical nutrient interaction. exposure: CuCl2 or FeCl2 exposure; NFE2L2 or ATOX1 knockdown evidence_span: {"source_cache": "artifacts/copper-research/40944334.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "6df1716e8998546d22a1d96116e1bc35b1f7e24c94868ec5e441ada6a2be3e89", "start_char": 0, "end_char": 1634, "text_sha256": "6df1716e8998546d22a1d96116e1bc35b1f7e24c94868ec5e441ada6a2be3e89"} [copper-p40944334] Copper induces cystine/glutamate antiporter SLC7A11 through the activation of Nrf2 and Atox1 pathways. (2025). https://pubmed.ncbi.nlm.nih.gov/40944334/ DOI: 10.1080/10715762.2025.2560847
    Complete structured claim and evidence

  3. NRF2 knockdown suppressed copper-induced SLC7A11 expression.

    Human Nrf2 / NFE2L2 → Copper-exposure-induced SLC7A11 expression in human MDA-MB-231 cells source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/copper-research/40944334.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "6df1716e8998546d22a1d96116e1bc35b1f7e24c94868ec5e441ada6a2be3e89", "start_char": 0, "end_char": 1634, "text_sha256": "6df1716e8998546d22a1d96116e1bc35b1f7e24c94868ec5e441ada6a2be3e89"}
    experimental_model
    Copper and iron exposure with transcription-factor knockdown
    exposure
    CuCl2 or FeCl2 exposure; NFE2L2 or ATOX1 knockdown
    limitations
    One cancer-cell model. Expression changes do not prove increased glutathione synthesis, tumor progression, or a clinical nutrient interaction.
    nutrient_topic
    Copper research collection; topical membership is not evidence of a direct dietary effect. · Copper
    organism
    Human MDA-MB-231 breast cancer cells
    plain_language
    The stress-response regulator was part of the transporter-expression response.
    primary_references
    [copper-p40944334] Copper induces cystine/glutamate antiporter SLC7A11 through the activation of Nrf2 and Atox1 pathways. (2025). https://pubmed.ncbi.nlm.nih.gov/40944334/ DOI: 10.1080/10715762.2025.2560847
    tissue_or_cell_type
    Cellular amino-acid transport machinery

    Copper: transport, cuproenzymes, deficiency, excess and nutrient interactions (2026-09-17) · lines 1300–1311

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Copper and iron exposure with transcription-factor knockdown · source_derived_draft · unverified_draft

    ### copper-nrf2-slc7a11 NRF2 knockdown suppressed copper-induced SLC7A11 expression. Condition category: normal nutrient_topic: Copper research collection; topical membership is not evidence of a direct dietary effect. plain_language: The stress-response regulator was part of the transporter-expression response. organism: Human MDA-MB-231 breast cancer cells tissue_or_cell_type: Cellular amino-acid transport machinery experimental_model: Copper and iron exposure with transcription-factor knockdown limitations: One cancer-cell model. Expression changes do not prove increased glutathione synthesis, tumor progression, or a clinical nutrient interaction. exposure: CuCl2 or FeCl2 exposure; NFE2L2 or ATOX1 knockdown evidence_span: {"source_cache": "artifacts/copper-research/40944334.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "6df1716e8998546d22a1d96116e1bc35b1f7e24c94868ec5e441ada6a2be3e89", "start_char": 0, "end_char": 1634, "text_sha256": "6df1716e8998546d22a1d96116e1bc35b1f7e24c94868ec5e441ada6a2be3e89"} [copper-p40944334] Copper induces cystine/glutamate antiporter SLC7A11 through the activation of Nrf2 and Atox1 pathways. (2025). https://pubmed.ncbi.nlm.nih.gov/40944334/ DOI: 10.1080/10715762.2025.2560847
    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