Project description:Gene expression in THP-1 cells treated for 6 hours with CNT and GNP conjugated with LL-37, LL-37 spiked as well as free LL-37: Reference (Total RNA Mixture of all samples) vs. treated cells
Project description:LL-37, a 37-amino acid human-derived antimicrobial peptide, exhibits antiviral functions against multiple enveloped and non-enveloped viruses. We here report that the expression of the Stac is upregulated by LL-37 regardless of EV71 infection in Caco-2 colorectal adenocarcinoma cells. The treatment of LL-37 inhibits viral infection compared to the scramble(scr) control. In addition, LL-37 significantly upregulates the Stac expression in the presence or absence of EV71 infection, while the viral infection itself does not affect the expression of Stac. Take together, our data provide a novel mechanism of its antiviral activity for non-enveloped viruses, in which LL-37 modulates the host genes, interfering with the process of viral infection.
Project description:Colicin V (ColV)-like plasmids (ColVLPs) are virulence plasmids frequently carried by extra-intestinal pathogenic E. coli (ExPEC) that cause human and avian infection. ColVLPs encode OmpTp, an outer membrane protease with the capacity to cleave the antimicrobial peptide LL-37, which is expressed in the human urinary tract. Homologs of OmpTp also exist on the E. coli chromosome, and differences in enzyme activity and cleavage profiles are largely uncharacterised. For this section of the project, the capacity of each OmpT variant to cleave LL-37 is tested, by incubating isogenic E. coli strains expressing each OmpT homolog with LL-37, and subsequently using LC-MS to quantify LL-37 cleavage products.
Project description:We examined the effects of ICG-001 on gene expression in Mel202 uveal melanoma (UM) cells. ICG-001 exerted strong antiproliferative activity against UM cells, leading to cell cycle arrest, apoptosis, and inhibition of migration. Global gene expression profiling revealed strong suppression of genes associated with cell cycle proliferation, DNA replication, and G1/S transition. Gene set enrichment analysis revealed that ICG-001 suppressed Wnt, mTOR, and MAPK signaling. Strikingly, ICG-001 suppressed the expression of genes associated with UM aggressiveness, including CDH1, CITED1, EMP1, EMP3, SDCBP, and SPARC. Notably, the transcriptomic footprint of ICG-001, when applied to a UM patient dataset, was associated with better clinical outcome. Lastly, ICG-001 exerted anticancer activity against a UM tumor xenograft in mice.
