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The tumour necrosis factor-related apoptosis-inducing ligand (TRAIL) triggers the apoptosis of tumour cells. According to recent studies, a number of malignant tumours show resistance to TRAIL due to activation and overexpression of the Yes-associated protein (YAP) signal pathway. Objective: To construct a novel type of bacterial outer membrane vesicles (BEVs) based delivery system to inhibit the growth of oral squamous cell carcinoma (OSCC) cells. Methods: BEVs loaded with verteporfin (VPF)/TRAIL (BEVs–TRAIL/VPF) was prepared by ultracentrifugation and filtration. The expression of TRAIL was verified by BCA and transmission electron microscopy. High-performance liquid chromatography was used in determining the drug loading of VPF and drawing a release curve in vitro. MTT and Western blot were adopted to reveal the anti-tumour activity of BEVs–TRAIL/VPF in vitro. Results: The BEVs–TRAIL/VPF particles appeared round by having a well uniform size distribution of approximately 100 nm in diameter. BEVs–TRAIL and VPF were capable of dose-dependently inhibiting the proliferation of SCC25 cells, and the best inhibitory effect appeared at ratios of 5:1–10:1. At 100:5–100:15 ratios, BEVs–TRAIL/VPF had a lower IC50 than free BEVs–TRAIL+VPF group (pConclusion: the administration of TRAIL/VPF in a fixed ratio by BEVs displays a profound inhibitory effect on OSCC cells, providing a novel approach for the treatment of multidrug-resistant OSCC.

The present study aims at the preparation of a chitosan-PLGA-based proanthocyanidin from hawthorn fruit loaded nano-system (CS-PLGA-PHL) and investigate its inhibitory effect on SCC-25 cells and the related mechanisms. Methods: CS-PLGA-PHL nanocomposites were constructed by emulsion-solvent evaporation. The effect of CS-PLGA-PHL on the proliferation of human normal squamous epithelial hNOK cells were detected. The antitumor activity of CS-PLGA-PHL on SCC-25 cells were studied by cytotoxicity test, cell cycle and apoptosis analysis. The apoptotic protein and gene expression in SCC-25 cells was detected by western blotting and q-PCR. Results: The particle size distribution of CS-PLGA-PHL was narrow with an average of 177.60±41.00 nm. CS-PLGA-PHL did not show significant cytotoxicity to hNOK cells (IC50 > 50 μg/mL), with strong cytotoxicity to SCC-25 cells (IC50 = 1.21 μg/mL), which could block the G0/G1 phase of SCC-25 cells and increase the distribution of G2/M phase. Meanwhile, the apoptosis induction of CS-PLGA-PHL was higher than that of free PHL and PLGA-PHL group (P Conclusion: CS-PLGA-PHL nanocomposites can inhibit the cell cycle and promote apoptosis of SCC-25 cells by up regulating the expression of apoptosis-associated proteins and genes, suggesting that it has potential as a chemotherapeutic drug for the treatment of oral squamous cell carcinoma.

Background: Multidrug resistance (MDR) is one of the primary causes of tumor chemotherapy failure. Therefore, it is essential to uncover new drug treatment protocols. In the current study, employing chitosan (CS) and sodium tripolyphosphate (TPP) as carriers and cross-linking agents, the proanthocyanidins (PHL)/poly (lactic-co-glycolic acid) (PLGA) were encapsulated by emulsion solvent evaporation, through which the cationic CS-PLGA-PHL nanosystem was obtained. The effectiveness of CS-PLGAPHL on the invasion and migration of human oral squamous cell carcinoma cells was discussed, as were their potential mechanisms. Methods: A CS-PLGA-PHL nanosystem was constructed by emulsion-solvent evaporation. The size distribution, dispersion, and morphology were characterised by the laser particle size analyser and transmission electron microscope. Human oral squamous cell carcinoma drug-resistant cell lines SCC131/R and SCC-15/DDP were cultured in vitro. The two cell types were induced at different concentrations by CS-PLGA-PHL, after which a CCK⁃8 experiment was performed to determine the effect of CS-PLGAPHL on the proliferation of the two cell lines. The 50% inhibitory concentration (IC50) of CS-PLGAPHL was calculated at different time points. The transwell chamber experiment was performed to identify the effects of CS-PLGA-PHL on the migration and invasion of OSCC cells. The expression levels of MMP-2 and MMP-9 were detected by Western blot and q-PCR. objective: The preparation of nano system to reduce the proliferative activity of OSCC cells together with inhibit the migration, invasion and tumor growth of OSCC cells Results: CS-PLGA-PHL is well dispersed. The PDI appeared to be lowest when the mass ratio of chitosan to PLGA equaled 1:15. CS-PLGA-PHL exhibited a marked effect in inhibiting the proliferation of SCC131/R and SCC-15/DDP as well as the invasion and migration. CS-PLGA-PHL was able to downregulate the expression of MMP-2 and MMP-9 genes and proteins significantly in drug-resistant cell lines. Conclusion: CS-PLGA-PHL for oral squamous cell carcinoma has been successfully prepared to exert significant inhibition on the proliferation, invasion, and migration of OSCC cells. The mechanism involved was possibly related to the down-regulation of MMP-2 and MMP-9 expression by CS-PLGA-PHL. result: CS-PLGA-PHL is well dispersed. The PDI appeared to be lowest when the mass ratio of chitosan to PLGA equaled 1 ∶ 15. CS-PLGA-PHL exhibited a marked effect in inhibiting the proliferation of SCC-131/R and SCC-15/DDP as well as the invasion and migration. CS-PLGA-PHL of was able to downregulate the expression of MMP-2 and MMP-9 genes and proteins significantly in drug-resistant cell lines other: None

Additional file 1: Table S1. Primers used for quantitative RT-PCR. Table S2. Chemical composition and relative amounts of sesquiterpenoids from branches in two germplasm resources at 30 d after wounding stress. Table S3. Sequencing and mapping statistics for the 12 transcriptomes data. Table S4. Enriched KEGG pathways in two germplasm resources comparisons. Table S5. DEGs were enriched in KEGG pathways in green, turquoise and red modules.