ArticleMolecular biomedicine2025
Delta-like ligand 4 mediated myeloid-derived suppressor cell metabolic reprogramming promotes neoadjuvant therapy resistance in titin-inactivated triple-negative breast cancer.
Article in Molecular biomedicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Tumor-infiltrating lymphocytes in triple-negative breast cancer: molecular mechanisms, spatial regulation, and therapeutic implications.Breast cancer research : BCR · 2026Review
- Lysine Acetyltransferase 6A Drives M1 Macrophage Polarization Through Metabolic Reprogramming in Sepsis-Induced Acute Lung Injury.Biomolecules · 2026Article
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Authors and funding
11 authors.
Funding
Abstract
Triple-negative breast cancer (TNBC) is characterized by complex genomic background and treatment resistance. We first defined "Titin (TTN) inactivation", a state of TTN expression deficiency or mutation, affecting tumor progression. However, how TTN inactivation regulates immune escape and affects therapeutic resistance remains unclear. Using whole-exome sequencing, single-cell transcriptome sequencing, and spatial transcriptome sequencing, we screened the clinical features of TNBC patients with TTN inactivation who accepted neoadjuvant therapy. Meanwhile, we used CRISPR-Cas9 technology to construct various mutant TNBC cell lines. Lentiviral vector carrying TTN and delta-like ligand 4 (DLL4) was validated in vivo to verify potential mechanism. Myeloid-derived suppressor cells (MDSCs) metabolic function was measured using glycolysis-related molecular experiments. Immunotherapeutic agents against TNBC with TTN inactivation were explored in the orthotopic MCT4
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