The poor prognosis and high recurrence rate of ovarian cancer highlight the urgent need to develop new therapeutic strategies. Oncolytic Newcastle disease virus (NDV) can kill cancer cells directly and regulate innate and adaptive immunity. In this study, ovarian cancer cells infected with or without velogenic NDV-BJ were subjected to a CCK-8 assay for detecting cell proliferation, flow cytometry for detecting the cell cycle and apoptosis, and wound healing and transwell assays for detecting cell migration and invasion. Transcriptomic sequencing was conducted to identify the differentially expressed genes (DEGs). GO and KEGG enrichment analyses were performed to explore the mechanism underlying the oncolytic effect of NDV on ovarian cancer cells. The results showed that infection with NDV inhibited ovarian cancer cell proliferation, migration, and invasion; disrupted the cell cycle; and promoted apoptosis. Compared with those in negative control cells, the numbers of upregulated and downregulated genes in ovarian cancer cells infected with NDV were 1,499 and 2,260, respectively. Thirteen KEGG pathways related to cell growth and death, cell mobility, and signal transduction were significantly enriched. Among these pathways, 48 DEGs, especially SESN2, HLA B/C/E, GADD45B, and RELA, that may be involved in the oncolytic process were screened, and qPCR analysis verified the reliability of the transcription data. This study discovered some key pathways and genes related to oncolytic NDV-induced phenotypic changes in ovarian cancer cells, which will guide our future research directions and help further explore the specific mechanisms by which infection with NDV suppresses ovarian cancer development.
Synbiotics have become a new-age treatment tool for limiting the progression of metabolic dysfunction-associated steatotic liver disease; however, inclusive comparisons of various synbiotic treatments are still lacking. Here, we have explored and evaluated multiple synbiotic combinations incorporating three distinctive prebiotics, lactitol, lactulose and fructooligosaccharides. Of the synbiotic treatments evaluated, a combination of fructooligosaccharides and probiotics (FOS+Pro) exhibited superior protection against western diet-induced liver degeneration. This synbiotic (FOS+Pro) combination resulted in the lowest body weight gains, liver weights and liver/body weight ratios. The FOS+Pro synbiotic combination substantially alleviated liver histopathological markers and reduced serum AST and cholesterol levels. FOS+Pro ameliorated hepatic inflammation by lowering expression of proinflammatory markers including TNF-α, IL-1β, IL-6, and CCL2. FOS+Pro significantly improved steatosis by restricting the expression of lipid metabolic regulators (ACC1, FAS) and lipid transporters (CD36) in the liver. These findings are critical in suggesting that synbiotic treatments are capable of restraining western diet-induced metabolic dysfunction in the liver. Additionally, this study demonstrated that adding probiotic strains amplified the effectiveness of fructooligosaccharides but not all prebiotics.
Citations
Citations
Citations
Citations
Citations
Citations
Citations
Citations
Citations
Citations
Citations
Citations