Background: Inflammation is a critical component of tumor progression and many cancers arise from sites of infection, chronic injury, and inflammation, where immune cells secrete large amounts of pro-inflammatory cytokines able to recruit a wide range of immune cells. The aim of this study was to gain insights into the molecular basis of potential chemo preventive and therapeutic activities of the -3 fatty acid DHA. Methods and Materials: Human umbilical vein endothelial cells (HUVEC) were treated with 50 μmol/L DHA for 48 hours and then stimulated with 5 ng/mL IL-1β for 3 hours. Total RNA from treated cells and controls were extracted using the RNeasy mini kit from Qiagen. RNA samples were analyzed quantitatively and qualitatively with a NanoDrop Spectrophotometer and an Agilent Bioanalyzer. RNA was labeled using Agilent low RNA Input Fluorescent Linear Amplification kit and purified by Qiagen’s RNeasy mini spin column. Gene expression profile was then performed using an Agilent Whole Human Genome Oligo Microarray, covering 41K unique genes and transcripts. Slides were scanned and image data processed using the Agilent Feature Extraction software. The raw data were processed by GeneSpring® 10 and differentially expressed RNA identified with the Benjamini and Hochberg False Discovery Rate (p<0.05) test. Functional and network analyses were performed by Ingenuity Pathways version 8.0 Analysis. Results and Conclusion: The gene expression profile of HUVEC pre-treated with DHA and stimulated with IL-1 shows that fish oil regulates several cellular pathways. Among these DHA down regulates the expression of 18 genes associated to cancer. In particular DHA affects the expression of HSPB8 and SIK1, known to be associated with breast cancer and the down regulation of PDE5A and DNAJA1 involved in colorectal cancer. The outcome of this study is of great interest because of DHA implication in human breast and colorectal cancer prevention.

The omega-3 fatty acid DHA down regulates the expression of genes associated with breast and colorectal cancers a whole–genome microarray analysis.

MARTINELLI, ROSANNA
2010-01-01

Abstract

Background: Inflammation is a critical component of tumor progression and many cancers arise from sites of infection, chronic injury, and inflammation, where immune cells secrete large amounts of pro-inflammatory cytokines able to recruit a wide range of immune cells. The aim of this study was to gain insights into the molecular basis of potential chemo preventive and therapeutic activities of the -3 fatty acid DHA. Methods and Materials: Human umbilical vein endothelial cells (HUVEC) were treated with 50 μmol/L DHA for 48 hours and then stimulated with 5 ng/mL IL-1β for 3 hours. Total RNA from treated cells and controls were extracted using the RNeasy mini kit from Qiagen. RNA samples were analyzed quantitatively and qualitatively with a NanoDrop Spectrophotometer and an Agilent Bioanalyzer. RNA was labeled using Agilent low RNA Input Fluorescent Linear Amplification kit and purified by Qiagen’s RNeasy mini spin column. Gene expression profile was then performed using an Agilent Whole Human Genome Oligo Microarray, covering 41K unique genes and transcripts. Slides were scanned and image data processed using the Agilent Feature Extraction software. The raw data were processed by GeneSpring® 10 and differentially expressed RNA identified with the Benjamini and Hochberg False Discovery Rate (p<0.05) test. Functional and network analyses were performed by Ingenuity Pathways version 8.0 Analysis. Results and Conclusion: The gene expression profile of HUVEC pre-treated with DHA and stimulated with IL-1 shows that fish oil regulates several cellular pathways. Among these DHA down regulates the expression of 18 genes associated to cancer. In particular DHA affects the expression of HSPB8 and SIK1, known to be associated with breast cancer and the down regulation of PDE5A and DNAJA1 involved in colorectal cancer. The outcome of this study is of great interest because of DHA implication in human breast and colorectal cancer prevention.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11386/3037714
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