Browsing by Subject "SW620"

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    Investigation of the effects of nicotine and levamisole on SW620 colon adenocarcinoma cells using a customized r-routine for automated microarray analysis
    (2010) Üçal, Muammer
    Nicotine, the addictive component of tobacco, shows proliferative and antiapoptotic activity in cancer cells. Levamisole, an antihelmintic, on the other hand, has been tested as an additive chemotherapeutic agent and in treatment of nephrotic syndrome. Nicotine and levamisole are both agonists of nicotinic acetylcholine receptors; effects of these two agents have not been studied in colon cancer transcriptome. In this study, nicotine and levamisole exposed SW620 colon cancer cells, at a dose of 1 μM for 7 days, were studied with respect to changes in expression using microarrays. For data analysis, a custom R-routine which makes extensive use of open source R-BioConductor Project and associated packages has been written; and it is composed of three modules: QualCont module performs quality controls supported with several visual
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    ItemOpen Access
    Investigation of the effects of nicotine on the expression profile of SW620 colon adenocarcinoma cells using a functional genomics approach
    (2009) Kaya, Onur
    Colon cancer is the third most common form of cancer with approximately 655,000 deaths worldwide annually and the second principal cause of cancer-related death in the Western world. Studies focusing on genomic instability and cell culture in recent years have shown that there is a statistically significant link between tobacco smoking and colorectal cancer. Although nicotine is one of the most potent chemical in tobacco, it was not studied extensively in colorectal cancers. Nicotine works as an agonist of nicotinic acetylcholine receptors and modulates the intracellular calcium concentrations hence deregulating multiple signal transduction pathways (e.g., PI3K/AKT, MAPK, mTOR). It has been shown that nicotine accelerates cell proliferation while it increases cell migration, metastasis and angiogenesis, and inhibits apoptosis in lung and gastric cancers. The aim of this study was to give more insight into the association between nicotine and colon cancer by investigating the gene expression profiles of SW620 colon adenocarcinoma cells under 48h 1µM nicotine treatment at different serum levels to reflect molecular response to growth factor-induced and –depleted conditions (10% FBS or 0.1% FBS). We used multiple approaches including cell culture techniques, microarray technology, and gene-network analysis to assess the effects of nicotine on cell proliferation and transcriptome profile. Furthermore, the selected genes that are involved in cell cycle and apoptosis were used to confirm and evaluate the transcriptome analysis results with real time qRT-PCR and Western Blot techniques. In this project, our findings indicated that serum starvation of SW620 colon adenocarcinoma cell line resulted in decreased cell proliferation, which could be rescued by 1µM nicotine via deregulation of multiple pathways including cell cycle, apoptosis, Ca2+ signaling, and ribosomal protein expression. This study implicated that nicotine-, thus acetylcholine-mediated signaling may have an important role in tumor development and metastasis.