Project description:Pancreatic cancer is one of the most deadly malignant tumors, and its treatment is scarce. This study found that arachidonic acid can induce pyroptosis of pancreatic cancer both in vitro and in vivo, and can cause immune cell infiltration. Arachidonic acid can be used as a tumor killing drug and an immunotherapy activator, which provides a new idea for the treatment of pancreatic cancer.
Project description:We performed HDAC5 knockdown in pancreatic cancer cells along with RNA sequencing. The result helped us to verify that HDAC5 regulates GATA1 dependent cPLA2 expression and arachidonic acid metabolism.
Project description:Unlike class I Histone deacetylase (HDAC) members (HDAC1, 2, 3, etc.), HDAC5, a class IIa HDAC member, is downregulated in multiple solid tumors, including pancreatic cancer, and its loss is associated with unfavorable prognosis. Additionally, HDAC5’s expression correlates negatively with arachidonic acid (AA) metabolism, which is highly implicated in inflammatory responses and cancer progression. This study aimed to elucidate the role of HDAC5 in AA metabolism and its prospect in the treatment of pancreatic cancer.
Project description:Although Candida species, more specifically C. albicans, are the most common pathogenic yeasts, little is known about the mechanism involved in eicosanoid production, a virulence factor in these organisms. This is an important area of research which may aid in the understanding of the complex interactions between host and pathogen and may possibly lead to the identification of novel antifungals or drug targets. In this study, genomic hybridization studies using C. albicans DNA microarrays were used to evaluate the regulation of C. albicans biofilm genes during incubation in the presence of arachidonic acid, the major precursor for prostaglandin E2 production. The results obtained indicated that the genes differentially expressed had diverse functions not normally required for cell growth. Two-condition experiment, Control biofilms vs. Arachidonic acid treated biofilms at different time intervals. Biological replicates: 3 Control, 3 Arachidonic acid treated, independently grown and harvested. Technical replicate: dye swap included. Triplicate per array.
Project description:Candida albicans is a commensal yeast within the human microbiota with significant medical importance because of its pathogenic potential. The yeast produces biofilms, which are highly resistant to available antifungals. High level of antifungal resistance by C. albicans biofilms has resulted in the need for alternative treatment. Polyunsaturated fatty acids such as arachidonic acid has been reported to increase the susceptibility of C. albicans biofilms to azole. However, the underlining mechanism is unknown. To unravel the mechanism behind this phenomenon, identification of differentially regulated genes in C. albicans biofilms grown in the presence of arachidonic acid, fluconazole, and the combination of both compounds was conducted using RNAseq.
Project description:Natural killer cells were exptracted from PMBCs of healthy donors, exposed to arachidonic acid, Il-2, both, or ascites and their expression changes identified via RNAseq (QuantSeq).