Show simple item record

dc.contributor.advisorÖztürk, Mehmet
dc.contributor.authorDemirdizen, Engin
dc.date.accessioned2016-01-08T20:06:30Z
dc.date.available2016-01-08T20:06:30Z
dc.date.issued2013
dc.identifier.urihttp://hdl.handle.net/11693/17096
dc.descriptionAnkara : The Department of Molecular Biology and Genetics and the Graduate School of Engineering and Science of Bilkent Univ., 2013.en_US
dc.descriptionThesis (Master's) -- Bilkent University, 2013.en_US
dc.descriptionIncludes bibliographical references leaves 90-94.en_US
dc.description.abstractBeing one of the most common cancer types in human population, hepatocellular carcinoma (HCC) has high rate of deaths due to the challenges in its diagnosis and treatment. In recent years, epigenetic regulators have come into play in HCC research to overcome with those challenges. As potential drug targets, histone demethylases has drawn a lot of interest. In this respect, several studies have focused on a specific member of this family, JMJD5, suggesting its possible function in tumor suppression, while the opposite argument has also been proposed by several reports. Preceding studies on JMJD5 in our lab also pointed to a possible tumor suppressor function. Hence, this study aimed to elucidate the role of JMJD5 in liver cancer development using SNU449 HCC cell line stably expressing JMJD5. For this purpose, stable clones overexpressing wild-type and mutant JMJD5 as well as controls were generated. A comparative analysis of these clones was performed. No definite results could be obtained for the effect of JMJD5 on cell proliferation, but the number of cells in G1 declined, whereas that in G2/M inclined in clones expressing wild-type and mutant JMJD5, suggesting that JMJD5 affects cell cycle progression. In addition, cell motility was decreased, while anchorage-independent colony formation ability was enhanced in both mutant and wild type JMJD5- expressing clones. Decrease in cell motility is considered to be anti-tumoral, whereas anchorage-independent growth is a malignant change. Our findings suggest that JMJD5 may have a quite complex role in liver tumorigenesis. Further in vivo studies may help to clarify some of these apparently conflicting in vitro effects.en_US
dc.description.statementofresponsibilityDemirdizen, Enginen_US
dc.format.extentxiv, 94 leaves, illustrations, graphicsen_US
dc.language.isoEnglishen_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.subjectJMJD5en_US
dc.subjectliver canceren_US
dc.subjecthepatocellular carcinomaen_US
dc.subjecttumor suppressoren_US
dc.subject.lccWI735 .D45 2013en_US
dc.subject.lcshCarcinoma, Hepatocellular.en_US
dc.subject.lcshLiver cancer.en_US
dc.titleRole of JMJD5 in liver canceren_US
dc.typeThesisen_US
dc.departmentDepartment of Molecular Biology and Geneticsen_US
dc.publisherBilkent Universityen_US
dc.description.degreeM.S.en_US


Files in this item

Thumbnail

This item appears in the following Collection(s)

Show simple item record