The improved anticancer effects of Bortezomib-loaded hollow mesoporous silica nanospheres on lymphoma development

As the first clinical proteasome inhibitor, Bortezomib (BTZ) has been reported to improve the outcome of lymphoma. However, due to the unstable property, low bioavailability, and hydrophobic properties of BTZ, it is needed to develop effective drug delivery systems to deliver BTZ into targeted cells or organs. Here we developed a bortezomib (BTZ)-loaded HMSNs (BTZ@HMSNs) system, which can sustain the release of BTZ in targeted tissues. In vitro assays showed that BTZ@HMSNs limited cell proliferation and augmented apoptosis of lymphoma SNK-1 cells. Moreover, BTZ@HMSNs significantly diminished migration and invasion of SNK-1 cells as compared with BTZ. In contrast to the upregulation of SHP-1, BTZ@HMSNs decreased the mRNA levels of cKit, NF-kappa B, and JAK1, which elicit oncogenic role in lymphoma development. Importantly, lymphoma mice model showed that BTZ@HMSNs significantly activated p53 signaling and reduced tumor volume and weight compared with free BTZ. Our data thus demonstrate that BTZ@HMSNs manifests improved tumor-suppressing effect in vitro and in vivo compared to free BTZ. We believe that HMSNs is a promising strategy for delivering therapeutic agents for cancer treatment.

Automated summary

Bortezomib-loaded HMSNs (BTZ@HMSNs) system sustains the release of BTZ, inhibits lymphoma cell proliferation and migration, and promotes apoptosis. BTZ@HMSNs downregulate oncogenic genes in lymphoma development, activate p53 signaling, and reduce tumor volume in lymphoma mice model, demonstrating improved tumor-suppressing effect compared to free BTZ. HMSNs show promise as a strategy for delivering therapeutic agents for cancer treatment.