Neutrophil mediated postoperative photoimmunotherapy against melanoma skin cancer.

Surgery is the primary treatment option for most melanoma; however, high tumor recurrence rate after surgical resection becomes the main cause of death in cancer patients. The development of efficient drug delivery nanosystems to inhibit postoperative tumor recurrence becomes very necessary. In the present study, IR780 molecules and TRP-2 peptide were encapsulated in the hydrophobic shell and hydrophilic interior of TAT peptide functionalized liposomes to form TLipIT NPs, which were further internalized into neutrophils (NEs) to achieve TLipIT/NEs. After being intravenously injected into postoperative B16F10-bearing mice, TLipIT/NEs could actively migrate toward the inflamed residual tumor and release TLipIT through neutrophil extracellular traps (NETs). Under NIR laser irradiation, the TLipIT exhibited both photothermal and photodynamic effects to induce immunogenic cell death for maturation of DCs, and simultaneously, to release TRP-2 peptide as a melanoma associated antigen to further strengthen the maturation of DCs, both of which prompts the activation of T cells and induces potent immune responses. TLipIT/NEs hold great potential for the inhibition of postoperative tumor recurrence.

Improving the photothermal therapy efficacy and preventing the surface oxidation of bismuth nanoparticles through the formation of a bismuth@bismuth selenide heterostructure.

Bismuth (Bi) nanoparticles (NPs) are emerging as promising photothermal agents for computed tomography imaging-guided photothermal therapy. However, it is challenging to improve their photothermal conversion efficacy and prevent their oxidation. Herein, Bi@bismuth selenide (Bi2Se3) core@shell NPs were designed and fabricated for improving the photothermal performance due to the staggered energy levels between Bi and Bi2Se3. With near-infrared light irradiation, both the materials could be excited to generate hot carriers due to their extremely narrow bandgaps. The hot electrons would transfer to the conduction band of Bi2Se3 and the hot holes to the valence band of Bi, leading to the effective separation of hot carriers. Then, these hot electrons and holes would recombine nonradiatively at the interface of Bi and Bi2Se3 and produce more phonons, resulting in an enhanced photothermal conversion efficacy. Moreover, the presence of Bi2Se3 on the surface of Bi NPs could prevent Bi from surface oxidation due to the higher stability of Bi2Se3. In fact, Bi@Bi2Se3 NPs showed excellent biocompatibility and photothermal therapeutic efficacy against cancer cells.

Effects of Jiazhu decoction in combination with cyclophosphamide on breast cancer in mice.

OBJECTIVE: To investigate the therapeutic effects of Jiazhu decoction (JZD) in combination with cyclophosphamide (CTX) on the growth of breast cancer in mice and to explore the possible molecular mechanisms of action. METHODS: BALB/c mice were randomly divided into four groups of 10 (untreated model group, JZD group, CTX group, and JZD + CTX group) and subcutaneously injected with 4T1 mouse breast cancer cells. Tumors were allowed to establish for ~7 d before initiation of treatment with CTX (100 mg/kg every week by intraperitoneal injection) and/or JZD (0.015 mL of 1.65 g/mL crude drug, administered daily by gavage). The model group received equivalent volumes of vehicle on the same schedules. Tumor volumes were measured every 3 d. Mice were sacrificed after 3 weeks of treatment, and tumors were excised and subjected to RT-qPCR and western blot analysis to evaluate expression of the Wnt/ß-catenin signaling pathway components ß-catenin, c-Myc, and cyclin D1 at the mRNA and protein levels. RESULTS: The mean tumor volume was smaller and the growth rate was slower in the CTX and JZD + CTX groups compared with the model group (P < 0.05), and in the JZD + CTX group compared with the CTX and JZD groups (P < 0.05). Tumor growth was inhibited by 35.4% and 48.1% by CTX and JZD + CTX treatment, respectively (P < 0.001). The expression of ß-catenin, c-Myc, and cyclin D1 mRNA and protein in tumors was significantly lower in mice treated with JZD or JZD + CTX compared with the untreated mice (P < 0.05), and was significantly lower in mice treated with JZD + CTX compared with either JZD or CTX alone (P < 0.05). CONCLUSION: JZD inhibited the growth of mouse breast cancer cells in vivo, possibly by reducing the expression of ß-catenin, c-Myc, and cyclin D1. Combination therapy with JZD plus CTX had a more potent inhibitory effect on breast cancer growth compared with either agent alone.