Project description:Sea buckthorn (Hippophae rhamnoides L.) is an economically important shrub or small tree indigenous to Asia and Europe. The most well-recognized medicinal and nutraceutical products derive from the berry oil, which is rich in essential fatty acids, monounsaturated palmitoleic acid (16:1 ω-7), linoleic (18:2 ω-6) and alpha-linolenic (18:3 ω-3) acids. In this study, tandem mass tags (TMT) MS/MS were used to investigate protein profiles of lipid metabolism in sea buckthorn berries harvested at 30, 50 and 70 days after flowering. A total of 8626 proteins were detected and 6170 of these were quantified. Further analyses of the proteins and their pathways revealed initiation of fatty acid accumulation throughout the whole berry development. Activity of most of key enzymes, which are related to biosynthesis pathways of triacylglycerol and fatty acids, had peaked at 50 days; but triacylglycerol synthesis through the PDAT (phospholipid: diacylglycerol acyltransferase) catalytic pathway of occurred mostly at the early stage of berry development. Protein expression patterns related to lipid accumulation were also verified at the transcript level using quantitative real-time polymerase chain reaction. The proteome profiles determined here will improve our understanding of the process of lipid accumulation and the dynamic changes in metabolic pathways during sea buckthorn berry development.
Project description:Fruits of sea buckthorn have abundant antioxidants and attractive colors. They provide excellent materials to study the relationships among fruit color, antioxidant and fruit quality
Project description:Sea buckthorn (Hippophae rhamnoides L.) is well adapted to extreme temperatures ranging from −43 to 40°C and is ideal material to study mechanisms related to low-temperature stress tolerance
Project description:TH2 and innate lymphoid cells 2 (ILC2) can stimulate tumor growth by secreting pro-tumorigenic cytokines such as IL4, IL5 and IL13. However, the mechanisms by which type 2 immune cells traffic to the tumor microenvironment (TME) are unknown. Here, in pancreatic ductal adenocarcinoma (PDAC), we show that oncogenic KrasG12D (Kras*) increases the expression of IL33 in cancer cells, which upon secretion recruits and activates the TH2 and ILC2. Correspondingly, cancer cell-specific deletion of IL33 reduces TH2 and ILC2 recruitment and promotes tumor regression. Unexpectedly, we discovered that the cellular release of IL33 into the TME is dependent on the intratumoral fungal mycobiome. Genetic deletion of IL33 or anti-fungal treatment decreases TH2 and ILC2 infiltration and increases survival. Consistent with these murine data, high IL33 expression is observed in approximately 20% of human PDAC, and expression is mainly restricted to cancer cells. These data expand our knowledge of the mechanisms driving PDAC tumor progression and identifies therapeutically targetable pathways involving intratumoral mycobiome-driven secretion of IL33.
Project description:We report the RNAseq of mouse pancreatic cancer cell lines with Kras ON vs Kras OFF. TH2 and innate lymphoid cells 2 (ILC2) can stimulate tumor growth by secreting pro-tumorigenic cytokines such as IL4, IL5 and IL13. However, the mechanisms by which type 2 immune cells traffic to the tumor microenvironment (TME) are unknown. Here, in pancreatic ductal adenocarcinoma (PDAC), we show that oncogenic KrasG12D (Kras*) increases the expression of IL33 in cancer cells, which upon secretion recruits and activates the TH2 and ILC2. Correspondingly, cancer cell-specific deletion of IL33 reduces TH2 and ILC2 recruitment and promotes tumor regression. Unexpectedly, we discovered that the cellular release of IL33 into the TME is dependent on the intratumoral fungal mycobiome. Genetic deletion of IL33 or anti-fungal treatment decreases TH2 and ILC2 infiltration and increases survival. Consistent with these murine data, high IL33 expression is observed in approximately 20% of human PDAC, and expression is mainly restricted to cancer cells. These data expand our knowledge of the mechanisms driving PDAC tumor progression and identifies therapeutically targetable pathways involving intratumoral mycobiome-driven secretion of IL33.