Resident tissue macrophages concentrated at the margins of pancreatic tumors play a crucial role in promoting cancer progression and epithelial-mesenchymal transition by supplying the selenium-transporting protein Selenop. This macrophage-derived Selenop is taken up by invasive tumor cells through an LRP8-dependent mechanism, which elevates cellular selenium availability and shields vulnerable mesenchymal cancer cells from lipid peroxidation and ferroptosis. Consequently, the targeted depletion of resident tissue macrophages or the disruption of this selenium axis significantly curtails tumor growth, limits metastasis, and prolongs survival in both mouse models and human pancreatic ductal adenocarcinoma patients.
References:
Guo W, Li Z, Chen Q, et al. Resident tissue macrophages transfer selenium transporter protein to protect pancreatic cancer from ferroptosis[J]. Cell, 2026.
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