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Tumor CTR1 Expression and Systemic Copper Dynamics Converge on a Copper Axis in High-Grade Triple-Negative Breast
Vinit Shanbhag1, Nikita S Gudekar1, Muhammad Yasir2
1Department of Biochemistry, Life Sciences Center, University of Missouri, Columbia, Missouri.
Cancer Research Communications
|June 10, 2026
Summary
Copper transporter 1 (SLC31A1) expression and serum copper changes are linked to breast cancer aggressiveness. Elevated SLC31A1 and post-treatment copper increases in triple-negative breast cancer (TNBC) suggest a copper mobilization program associated with neoadjuvant resistance.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Copper metabolism is crucial in cancer, with CTR1 (SLC31A1) mediating cellular copper uptake.
- The role of SLC31A1 and systemic copper dynamics in breast cancer aggressiveness and neoadjuvant treatment response remains unclear.
Purpose of the Study:
- To investigate the coordinated relationship between tumor SLC31A1 expression and systemic copper dynamics in breast cancer.
- To determine if this axis reflects tumor aggressiveness and response to neoadjuvant therapy.
Main Methods:
- Retrospective analysis of tumor SLC31A1 gene expression in 1,632 neoadjuvant-treated breast cancer patients, stratified by response, subtype, and grade.
- Prospective assessment of serum copper changes (△Copper) in relation to subtype, grade, response, and tumor size.
Main Results:
- Higher baseline SLC31A1 expression was observed in triple-negative breast cancer (TNBC) non-responders, particularly in grade 3 tumors.
- △Copper changes were most pronounced in TNBC and were grade-dependent, with grade 3 showing copper elevation and grade 2 showing decreases post-therapy.
- Persistent positive △Copper was noted in relapsed TNBC non-responders, unlike other subtypes.
Conclusions:
- Elevated baseline tumor SLC31A1 expression and post-therapy systemic copper increases are associated with high-grade TNBC.
- These findings suggest a coordinated copper mobilization program linked to aggressive biology and neoadjuvant resistance in TNBC.
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