Component

Hypoxic proliferation of human cancer cells

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

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. Increasing SLC1A3-mediated uptake supplied aspartate for nucleotide synthesis and improved proliferation under low oxygen and growth in tumor xenograft models.

    Experimental context and source evidence
    evidence_access
    Primary full text
    experimental_model
    Human cancer cultures and xenografts in immunodeficient mice.
    limitations
    Not every tumor expresses this transporter, and this is not evidence that ordinary intake initiates cancer. Correction record: The 2018 author correction added a missing competing-interests statement declaring no competing interests; no mechanism or data change was stated. PMID 30089842; DOI 10.1038/s41556-018-0184-2. https://pubmed.ncbi.nlm.nih.gov/30089842/
    nutrient_topic
    L-Aspartate collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Aspartate
    plain_language
    Uptake partly bypassed a synthesis bottleneck in the tested tumors.
    primary_references
    Aspartate is a limiting metabolite for cancer cell proliferation under hypoxia and in tumours. · 2018 · https://pubmed.ncbi.nlm.nih.gov/29941933/ · DOI 10.1038/s41556-018-0118-z

    L-Aspartate: redox transfer, nitrogen partitioning and cross-nutrient mechanisms (2026-09-19) · lines 82–88

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human cancer cultures and xenografts in immunodeficient mice. · source_derived_draft · unverified_draft

    ## l-aspartate-eaat1-hypoxia Uptake partly bypassed a synthesis bottleneck in the tested tumors. Increasing SLC1A3-mediated uptake supplied aspartate for nucleotide synthesis and improved proliferation under low oxygen and growth in tumor xenograft models. Model: Human cancer cultures and xenografts in immunodeficient mice. Limitations: Not every tumor expresses this transporter, and this is not evidence that ordinary intake initiates cancer. Correction record: The 2018 author correction added a missing competing-interests statement declaring no competing interests; no mechanism or data change was stated. PMID 30089842; DOI 10.1038/s41556-018-0184-2. https://pubmed.ncbi.nlm.nih.gov/30089842/ Evidence access: Primary full text Aspartate is a limiting metabolite for cancer cell proliferation under hypoxia and in tumours. · 2018 · https://pubmed.ncbi.nlm.nih.gov/29941933/ · DOI 10.1038/s41556-018-0118-z
    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