ArticleCell reports. Medicine2026
Comprehensive single-cell metabolic profiling identifies targets to sensitize triple-negative breast cancer to chemo-immunotherapy.
Article in Cell reports. Medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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Who cites it
2 citing papers in PubMed.
- Enzymatic activity-independent NANS stabilizes LATS2 to drive growth and therapeutic resistance in HR+/HER2- breast cancer.Nature communications · 2026Article
- Decoding the immunometabolic landscape identifies SLC7A5 as a vulnerability in chemo-immunotherapy resistant TNBC.Clinical and experimental medicine · 2026Article
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Authors and funding
8 authors.
Funding
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Abstract
The treatment of triple-negative breast cancer (TNBC) poses significant challenges, necessitating innovative approaches to identify therapeutic targets. This study presents a cohort of patients with early-stage TNBC receiving neoadjuvant chemotherapy or chemo-immunotherapy, leveraging single-cell RNA sequencing and metabolic analysis to elucidate the impact of metabolic reprogramming on treatment response. Our findings reveal metabolic heterogeneity at levels of metabolic genes, pathways, and fluxes. Cell-type-specific metabolic traits show stronger associations with therapeutic response compared with bulk metabolic features and the proportion of major cell types. We identify a dynamic collaboration between tumor cells and myeloid cells driven by differential glucose utilization and lactate production, which facilitates tumor progression. Monocarboxylate transporter 1 (MCT1) inhibitors disrupt their interaction, enhancing the efficacy of anti-PD-1 and antibody-drug conjugate (ADC) treatments in TNBC mouse models. Overall, our study delineates the single-cell metabolic landscape of TNBC and positions MCT1 as a promising target.
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