Bone metastasis along with osteolysis is a common complication of advanced breast cancer, which directly destroys bone function and becomes one of the major causes of cancer-related mortality. It is crucial to develop a new strategy to achieve effective cancer therapy and inhibition of osteolytic bone metastasis. Metal ruthenium (Ru) complexes exhibit therapeutic potential in cancer chemotherapy. However, the clinical applications of Ru complexes were limited by poor bioavailability, lacking targeting, nonspecific distribution. Therefore, in this study, engineering of cell membrane biomimetic modification was used to construct a highly biocompatible nanoplatform with carrying Ru metal complex of RuPOP and Se nanoparticles (SeNPs). Strikingly, the obtained RPSR nanoparticles can efficiently inhibit the proliferation, invasion and migration of breast cancer cells (MDA-MB-231 cells) in vitro. More importantly, RPSR nanoparticles can induce cycle arrest, apoptosis by generating excessive intracellular (reactive oxygen species, ROS) to disrupt the normal redox balance and induce DNA damage in tumor cells. Furthermore, RPSR nanoparticles can also reshape bone microenvironment by regulating selenoproteins to inhibit osteoclasts and avoid osteolytic bone metastasis induced by tumor development. Taken together, this study not only provides an effective cell membrane biomimetic strategy to enhance the shortcomings of metal complexes, but also demonstrates potential clinical significance for the combined treatment of anti-cancer and bone metastasis inhibition.

Circulating tumor cells (CTCs) are important biomarkers in the development and progression of lung cancer because they can reach other organs through the blood circulation and form distant metastases, exacerbating lung cancer progression. The presence of CTCs is also the main reason for the failure of nanomedicine-based lung cancer treatments. Therefore, magnetic MoSe₂ nanosheets loaded with programmed death-ligand 1 (PD-L1), named PD-L1-MFP NS, were employed here to precisely capture lung cancer CTCs in the blood circulation through the tumor-targeting effect of PD-L1 killing CTCs with highly effective photothermal therapy (PTT). In addition, by increasing the expression of cytomegalovirus UL16-binding protein (ULBP) ligands on tumor cells, the PD-L1-MFP NS further activated natural killer (NK) cells and triggered NK cell-induced cancer immunotherapy, thereby enhancing the overall tumor-killing effect. In summary, this material designed to capture CTCs provides a substantial advancement for personalized PTT-triggered immunotherapy and has great clinical translational potential.

Radiotherapy is one of the main therapeutic methods for cancers; however, nonselective killing of normal cells and tumor cells by X-ray inevitably results in toxicity and side effects. Developing low-toxicity and high-efficiency radiosensitizers to reduce the practical dose of X-ray is a promising approach to overcoming these side effects. Here, we report the use of carboxylate-containing organic ligands to construct one-dimensional high-Z lanthanide chains for efficient response to X-ray. The one-dimensional lanthanide chains are stacked through weak interactions to form coordination nanoframeworks in the presence of polyethylenimine (PEI). The morphology and activity of the synthesized nanoframeworks can be regulated through selenium atom engineering. This study presents a promising approach for effective radiotherapy through selenium-engineering stable lanthanide nanoframeworks with precise coordination structures as radiosensitizers to mitigate X-ray side effects.