Project description:KYSE510 cells were treated with 100 nM PAF for 24 hours,and then KYSE510 cells were collected for gene expression analysis using Agilent SurePrint G3 Human Gene Expression v3 (8×60K) Microarray. Investigation of the gene network of KYSE510 cells regulated by PAF.
Project description:primary lung fibroblasts p3 from normal periphery of resected cancer. grown in DMEM 10% FBS, until confluence, then DMEM 0.5% FBS for 18 hours. Media were then changed and incubated for an additional 4 hours in the presence or absence of 100 nM endothelin-1. Data represent two independent experiments performed on two different occasions. Keywords: other
Project description:AKGs enriched transcripts associated with PC-, lyso-PC and PAF metabolism. Moreover, AKGs suppressed interferon response genes. We submit heren three sets of NGS analyses. Experiment 1: We treated mouse adipose tissue macrophages (ATMs) with vehicle (ethanol) or 100 nM alkylglycerols (AKGs) for 18h in vitro. Experiment 2: We treated mouse 3T3-L1 preadipocytes with 1 nM neuropeptide FF (NPFF) for 18 h. Experiment 3: we isolated white adipose tissue from C57Black/6 male mice at 8 weeks of age, and brown adipose tissue from the same mice.
Project description:Purpose: To fully realize the potential molecular mechanism that LHX2 promotes ESCC progression Methods: Total RNA of LHX2-knockdown KYSE30/KYSE510 and control cells was extracted with TRIzol Reagent. RNA libraries were constructed using an Illumina TruSeq RNA Sample Preparation kit according to the manufacturer’s protocol. A total of 150 base paired-end reads were sequenced using the Novaseq 6000 S4 platform. Results: We identified 26008 transcripts in KYSE30 control and KYSE30 LHX2-knockdown cells ,and 25561 transcripts in KYSE510 control and KYSE510 LHX2-knockdown cells. Conclusions: Our study represents the analysis of LHX2-knockdown ESCC cells, generated by RNA-seq.
Project description:New alkyl-phospholipids (APLs) that are structurally derived from the platelet-activating factor are promising candidates for anticancer treatment. After the incorporation into cell membranes, APLs are able to interfere with a wide variety of key enzymes implicated in cell growth, motility, invasion and apoptosis. Recently, using Agilent cDNA microarray technology, we could demonstrate that the glycosidated APL Ino-C2-PAF inhibited the expression of several genes associated with immune response and inflammation in immortalized keratinocytes HaCaT. Here, we analyzed the impact of Ino-C2-PAF on the gene expression profile of HaCaT cells treated with several pro-inflammatory cytokines (IL-1M-NM-1, IL-17, IL-22, TNF-M-NM-1 and oncostatin-M). The influence of Ino-C2-PAF on the transcriptional profile of immortalized keratinocytes (HaCaT) was analyzed treating HaCaT cells with 5 M-BM-5M Ino-C2-PAF in the presence of a mixture of pro-inflammatory cytokines (IL-1M-NM-1, IL-17, IL-22, TNF-M-NM-1 and oncostatin-M) for 24 h. Control cells were left untreated. Three independent experiments were performed for each condition, except for control cells where only two experiments were performed. Control cells were mainly necessary to demonstrate the efficiency of this in vitro inflammation model for keratinocytes.
Project description:The conserved Eukaryotic PAF complex binds to transcribing RNA polymerase II to control deposition of histone marks during transcription. Recently its role in alternative polyadenylation (selection of mRNA 3’end cleavage sites by CPSF) was described. In this work we show that the PAF complex also regulates alternative splicing.