Project description:Sulforaphane and sulforaphene are isothiocyanate compounds derived from cruciferous vegetables that have demonstrated antiproliferative properties against colon cancer. However, the underlying mechanism of action of these two compounds is yet to be elucidated. The present study aimed to study the effects of sulforaphane and sulforaphene on colon cancer by next-generation sequencing (NGS).
Project description:Two colon cancer cell lines are under study. SW480 and SW620. The first one is derived from primary cancer, SW620 are from lymphnode metastatic sites. they both comes from the sampe patient. Polisomal RNA fractions from the two isogenic colon cancer cells lines was purified by sucrose gradient and hybridized on affymetrix hgu133a chips. this study is complementary to the series GSE1323 were total RNA was used instead. Comparison between the polysomal fraction chips and the total RNA chips is performed and the analysis proposed in a paper from the authors (at the moment in preparation). Keywords: other
Project description:H460 cells treated with vehicle or sulforaphane (SFN) for 48 hours were used to acquire expression profiles of a total of 1891 unique miRNAs. We aimed at identifying the differentially expressed miRNAs between cells treated or untreated with SFN.
Project description:Protective roles of Nrf2, a key transcription factor for antioxidant and defense genes, have been determined in oxidative lung injury, and health benefits of Nrf2 agonists including sulforaphane have been demonstrated. The current study was designed to investigate the effect of sulforaphane on model acute lung injury and sulforaphane-mediated transcriptome changes in mouse lungs. Adult mice genetically deficient in Nrf2 (Nrf2-/-) and wild-type controls (Nrf2+/+, ICR) received oral sulforaphane (9 mmol/daily) or vehicle before (-5, -3, -1 days) hyperoxia or air exposure (3 days), and lung injury and gene expression changes were assessed. Sulforaphane significantly reduced hyperoxia-induced airway injury, inflammation, and mucus hypersecretion in Nrf2+/+ mice while relatively marginal treatment effect was found in Nrf2-/- mice. Sulforaphane significantly altered expression of lung genes associated with oxidative phosphorylation and mitochondrial dysfunction (Atp2a2, Cox7a1, Ndufa1) basally and cell function/cycle and protein metabolism (Actr1a, Wasf2, Ccne1, Gtpbp4) after hyperoxia in Nrf2+/+ mice. Nrf2-dependently modulated lung genes by sulforaphane and hyperoxia were associated with tissue development and hereditary disorders (Slc25a3, Pccb, Psmc3ip). Results demonstrate preventive roles of sulforaphane against oxidant lung injury in mice, and reveal potential downstream mechanisms. Our observations also suggest Nrf2-independent mechanisms of sulforaphane in prevention of acute lung injury.