Hui Feng

Tissue engineering holds great potential for tissue repair and rejuvenation. Plant-derived exosome-like nanoparticles (ELNs) have recently emerged as a promising avenue in tissue engineering. However, there is an urgent need to understand how plant ELNs can be therapeutically applied in clinical disease management, especially for tissue regeneration. In this review, we comprehensively examine the properties, characteristics, and isolation techniques of plant ELNs. We also discuss their impact on the immune system, compatibility with the human body, and their role in tissue regeneration. To ensure the suitability of plant ELNs for tissue engineering, we explore various engineering and modification strategies. Additionally, we provide insights into the progress of commercialization and industrial perspectives on plant ELNs. This review aims to highlight the potential of plant ELNs in regenerative medicine by exploring the current research landscape and key findings.

S1: SMAD4+/+ and SMAD4-/- colon cancer cells were serum-starved and seeded on transwells and allowed to cross the membrane for 24 hours (transwell migration; RFU, relative fluorescence unit; mean {plus minus} SD, n = 3 biological replicates; **P < 0.01). S2: RICTOR depletion in SMAD4-negative colon cancer cells using shRNA#2 was measured by RT-qPCR (RT-qPCR; mean {plus minus} SD, n = 3 technical replicates; ***P < 0.001). B, Western blotting shows the relative levels of RICTOR, p-AKTS473, and cleaved-caspase 3 upon knockdown of RICTOR and in response to irinotecan. C, The indicated cell lines were treated with irinotecan (10μM) for 72 hours. S3: Cells depleted of RICTOR were serum starved and seeded on transwells and allowed to cross the membrane for 24 hours (transwell migration; RFU, relative fluorescence unit; mean {plus minus} SD, n = 6 biological replicates; ***P < 0.001). S4: A, Western blot shows the relative levels of RICTOR and p-AKTS47 in SW403 cells upon transfection with the indicated siRNAs. B, siRNA-transfected SW403 cells were treated with irinotecan (10μM) for 120 hours. Viability of cells was normalized to DMSO-treated controls (cell viability assay; mean {plus minus} SD, n = 3 biological replicates; **P < 0.01). S5: High RICTOR/AKT1 expression correlates with worse survival in colon cancer. S6: Targeting AKT with MK2206 sensitizes SMAD4-negative SW403 colon cancer cells to irinotecan. S7: Targeting AKT with either AKTi-1/2 or MK2206 sensitizes SMAD4-negative colon cancer cells to irinotecan. S8: No toxicity observed in mice exposed to MK2206 and irinotecan. S9: Targeting AKT with MK2206 sensitizes SMAD4-negative ASPC1 and CFPAC1 pancreatic cancer cells to irinotecan. S10: In silico Kaplan-Meier analyses showing the correlation between SMAD4, RICTOR, or AKT1 expression and overall survival (OS) in pancreatic cancer patients.

PDF file - 98K, Supplementary Figure S4: Caspase activation by G6T8.

PDF file - 63K, Identification of BRAFV600E splice variant lacking exons 2-10 in dabrafenib resistant WMD009 tumour and derived cell line.

PDF file - 85K, Supplementary Figure S2: Specificity of TRAILR2-induced cell killing. TRAIL-sensitive cell lines were incubated with 100pM G6T8 and different concentrations of soluble TRAILR2-Fc fusion protein.

PDF file - 59K, Supplementary Figure S3: G6T8 is specific for human TRAILR2 and does not cross-react with other TRAIL receptors.

PDF file - 148K, Supplementary Figure S5: G6T8 and G6T6 have similar cytotoxic activity on TRAIL-sensitive cell lines.

Mosapride significantly improves intestinal motility in liver cirrhosis, ultimately leading to the reduction in plasma endotoxin levels and bacterial translocation. To investigate the effects of mosapride on intestinal microecology in cirrhotic rats and its potential mechanisms. Forty-five healthy male Sprague-Dawley rats that were pathogen-free (weight 200-220 g) were randomly divided into a control group (n = 15), model group (n = 15) and mosapride group (n = 15). Then, the pathological changes in the liver and intestine were determined through tissue staining and using transmission electron microscope (TEM). Bacterial translocation was examined. High throughput 16S rRNA sequencing was performed to determine the changes of gut microbiota in each group. Compared with the model group, mosapride treatment induced no attenuation in hepatic morphology and pathology changes. The TEM indicated no differences in intestinal structure in both groups. There was a significant decline in the rate of gut microbiota translocation in the mosapride group compared with the model group. There were intestinal microbiota changes in the mosapride group compared with that of the model group, including Bacteroidetes, Prevotellaceae, Alloprevotella, Ruminiclostridium, Negativicutes, Selenomonadales, Veillonellaceae, Anaerovibrio, Campylobacterales, Epsilonbacteraeota, Helicobacter, Oscillibacter, Verrucomicrobiales, Akkermansia, Intestinimonas, Eubacterium, Clostridiaceae, Clostridium, Bacteroides, Tyzzerella, Actinobacteria, and Bifidobacteriales. Among these bacteria, Alloprevotella showed a strong correlation with the other bacteria. Taken together, we concluded that mosapride may reduce intestinal bacterial translocation through regulating the gut microbiota in rats with hepatic cirrhosis.