Investigation of the effects of nicotine on the expression profile of SW620 colon adenocarcinoma cells using a functional genomics approach

Simple item page
buir.advisorKonu, Özlen
dc.contributor.authorKaya, Onur
dc.date.accessioned2016-01-08T18:17:00Z
dc.date.available2016-01-08T18:17:00Z
dc.date.issued2009
dc.departmentDepartment of Molecular Biology and Geneticsen_US
dc.descriptionAnkara : The Department of Molecular Biology and Genetics and the Institute of Engineering and Science of Bilkent University, 2009.en_US
dc.descriptionThesis (Master's) -- Bilkent University, 2009.en_US
dc.descriptionIncludes bibliographical references leaves 84-96.en_US
dc.description.abstractColon 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.en_US
dc.description.degreeM.S.en_US
dc.description.statementofresponsibilityKaya, Onuren_US
dc.format.extentxvii, 96 leaves, illustrationsen_US
dc.identifier.urihttp://hdl.handle.net/11693/15339
dc.language.isoEnglishen_US
dc.publisherBilkent Universityen_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.subjectNicotineen_US
dc.subjectnicotinic acetylcholine receptorsen_US
dc.subjectSW620en_US
dc.subjectcolon canceren_US
dc.subjectmicroarrayen_US
dc.subjectserum starvationen_US
dc.subject.lccQP801.N48 K39 2009en_US
dc.subject.lcshNicotine--Metabolism.en_US
dc.subject.lcshNicotine--Physiological effects.en_US
dc.subject.lcshColon (Anatomy)--Cancer.en_US
dc.titleInvestigation of the effects of nicotine on the expression profile of SW620 colon adenocarcinoma cells using a functional genomics approachen_US
dc.typeThesisen_US

Files

Original bundle
Now showing 1 - 1 of 1
Thumbnail Image
Name:
0006086.pdf
Size:
4.77 MB
Format:
Adobe Portable Document Format
Download

Collections

Dept. of Molecular Biology and Genetics - Master's degree