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Triple negative breast cancer (TNBC) is a heterogeneous disease and is highly related to immunomodulation. As we know, the most effective approach to treat TNBC so far is still chemotherapy. Chemotherapy can induce immunogenic cell death, release of damage-associated molecular patterns (DAMPs), and tumor microenvironment (TME) remodeling; therefore, it will be interesting to investigate the relationship between chemotherapy-induced TME changes and TNBC immunomodulation. In this review, we focus on the immunosuppressive and immunoreactive role of TME in TNBC immunomodulation and the contribution of TME constituents to TNBC subtype classification. Further, we also discuss the role of chemotherapy-induced TME remodeling in modulating TNBC immune response and tumor progression with emphasis on DAMPs-associated molecules including high mobility group box1 (HMGB1), exosomes, and sphingosine-1-phosphate receptor 1 (S1PR1), which may provide us with new clues to explore effective combined treatment options for TNBC.
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http://dx.doi.org/10.3390/cancers13133357 | DOI Listing |
PLoS One
September 2025
Cancer Research Institute, College of Medicine, The Catholic University of Korea, Seoul, Republic of Korea.
Crosstalk between leukemic cells and their surrounding mesenchymal stromal cells (MSCs) in the bone marrow microenvironment is crucial for the pathogenesis of myelodysplastic syndromes (MDS) and is mediated by extracellular vesicles (EVs). The EV-specific miRNAs derived from MDS-MSCs remain poorly explored. EVs isolated from HS-5, an immortalized stromal cell line, promoted the proliferation and 5-azacytidine (AZA) resistance of SKM-1 cells.
View Article and Find Full Text PDFAm J Physiol Cell Physiol
September 2025
Department of Cancer Biology, Wake Forest University School of Medicine, Winston-Salem, NC.
Cachexia, the loss of skeletal muscle mass and function with cancer, contributes to reduced life quality and worsened survival. Skeletal muscle fibrosis leads to disproportionate muscle weakness; however, the role of infiltrating immune cells and fibro-adipogenic progenitors (FAPs) in cancer-induced muscle fibrosis is not well understood. Using the C26 model of cancer cachexia, we sought to examine the changes to skeletal muscle immune cells and FAPs which contribute to excessive extracellular matrix (ECM) collagen deposition.
View Article and Find Full Text PDFClin Cancer Res
September 2025
University of Michigan-Ann Arbor, Ann Arbor, MI, United States.
Purpose: Liposarcoma (LPS) is the most common soft tissue sarcoma. Well-differentiated LPS (WDLPS) can progress to dedifferentiated LPS (DDLPS), a more aggressive form with higher metastatic potential and poor response to existing therapies. Progress in understanding and treating LPS has been limited.
View Article and Find Full Text PDFJ Am Chem Soc
September 2025
Frontiers Science Center for New Organic Matter, State Key Laboratory of Medicinal Chemical Biology, College of Life Sciences and Academy for Advanced Interdisciplinary Studies, Nankai University, Tianjin 300071, PR China.
Antigen-capturing nanomaterials hold great promise for cancer immunotherapy; however, the need for tumor localized administration and limited antigen-binding affinity remains the "Achilles heel" of this strategy. Herein, we present a tumor microenvironment (TME)-activatable nanoplatform, TDR848@FPB, designed for systemic administration and enhanced covalent capture of tumor-associated antigens (TAAs), enabling effective immunotherapy with minimal off-target effects and independent of localized tumor administration. This platform encapsulates a photosensitizer-conjugated, light-activated toll-like receptor (TLR) agonist, which induces immunogenic cell death and triggers a pro-inflammatory TME conducive to antigen capture upon light irradiation.
View Article and Find Full Text PDFCancer Res
September 2025
The Wistar Institute, Philadelphia, PA, United States.
Parkin is a mitochondria-associated E3 ubiquitin (Ub) ligase that mediates mitophagy and organelle quality control. More recently, Parkin has been implicated in stimulating antitumor immunity and reprogramming the tumor immune microenvironment. Here, we showed that Parkin ubiquitinates the alarmin molecule, high mobility group box-1 (HMGB1) on Lys146 (K146) using predominantly K48 linkages.
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