ReviewFrontiers in immunology2026
Mitochondrial transfer-mediated metabolic reprogramming and drug resistance in bone metastasis: mechanisms and therapeutic strategies.
Review in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Bone is one of the most common sites of distant metastasis in solid tumors, particularly breast cancer, prostate cancer, and lung cancer. Bone metastatic lesions frequently exhibit persistent resistance to multiple systemic therapies, including chemotherapy, targeted therapy, endocrine therapy, and immune checkpoint inhibitors (ICIs). Accumulating evidence suggests that metabolic reprogramming within the bone microenvironment contributes to this resistance, yet the upstream mechanisms remain incompletely understood. Intercellular mitochondrial transfer has emerged as a potential link between the bone marrow niche and tumor metabolic adaptation. Bone marrow mesenchymal stem cells (BMSCs) have been reported to deliver functional mitochondria to tumor cells through tunneling nanotubes (TNTs), extracellular vesicles (EVs), and gap junctions, a process proposed to be regulated by metabolic stress, chemokine signaling (CXCL12/CXCR4), and inflammatory cues. The bone marrow microenvironment-characterized by hypoxia, high cell density, and lipid abundance-together with the intrinsic transfer capacity of BMSCs, may facilitate efficient mitochondrial delivery. Following transfer, exogenous mitochondria have been shown, largely
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