Tools

LEADER 05136nam 2200589Ii 4500

001 ocn881502190;

003 OCoLC;

005 20141212070344.0;

006 m o d ;

007 cr bn|||||||||;

008 140619s2014 ncua ob 000 0 eng d;

035 a| (Sirsi) o881502190;

035 a| (OCoLC)881502190;

040 a| EREe| rdac| EREd| UtOrBLW;

049 a| EREE;

066 c| (S;

100 1 a| Nopparat, Jongdee,e| author.?| UNAUTHORIZED;

245 10 a| [Delta]-catenin: implications in prostate cancer progression /c| by Jongdee Nopparat.;

264 1 a| [Greenville, N.C.] :b| [East Carolina University],c| 2014.;

300 a| 218 pages :b| illustrations (some color);

336 a| textb| txt2| rdacontent;

337 a| computerb| c2| rdamedia;

338 a| online resourceb| cr2| rdacarrier;

347 a| text fileb| PDFc| 5.04Mb2| rda;

490 1 a| ECU Brody School of Medicine thesis;

538 a| System requirements: Adobe Reader.;

538 a| Mode of access: World Wide Web.;

502 b| Ph.D.c| East Carolina Universityd| 2014.;

500 a| Presented to the faculty of the Department of Anatomy and Cell Biology.;

500 a| Advisor: Yan-Hua Chen.;

500 a| Title from PDF t.p. (viewed June 18, 2014).;

504 a| Includes bibliographical references.;

500 a| Non-Latin script record;

650 2 a| Prostatic Neoplasmsx| diagnosis.=| ^A925814;

650 2 a| Cateninsx| metabolism.=| ^A1205397;

650 2 a| Adenocarcinomax| diagnosis.=| ^A1201778;

653 a| Molecular biology;

653 a| [delta];

700 1 a| Chen, Yan-Hua,e| degree supervisor.?| UNAUTHORIZED;

710 2 a| East Carolina University.b| Department of Anatomy and Cell Biology.?| UNAUTHORIZED;

830 0 a| ECU Brody School of Medicine thesis.=| ^A964744;

856 40 z| Access via ScholarShipu| http://hdl.handle.net/10342/4436;

880 3 6| 520-00/(Sa| Prostate cancer (PCa) is the most commonly diagnosed cancer and the second most common cause of cancer death among men in the US. Due to the advances in research, the ability to detect and cure PCa has improved and led to significant reductions in PCa patients' mortality. Therefore, determining and understanding specific molecular mechanisms involved in PCa progression is a pivotal step towards the potentially better and more accurate diagnosis and intervention of PCa in the future. [Delta]-catenin is a unique armadillo (Arm) domain containing protein in that it is neural specific and primarily expressed in the brain. However, [delta]-catenin alterations have been implicated in pathogenesis ranging from neuronal deficits, genetic disorders, to cancers. In particular, [delta]-catenin expression is shown to increase in primary human prostatic adenocarcinomas corresponding with PCa progression. Although overexpressed [delta]-catenin in PCa has been reported over a decade ago, few studies have been undertaken to identify how [delta]-catenin promotes PCa progression and what other significant molecules are relevant to its expression. Studies presented in this dissertation explore the effects of a truncated variant of [delta]-catenin involved in promoting PCa using both in vitro PCa culture systems and in vivo mouse models of PCa. Additionally, we aim to test the hypothesis that [delta]-catenin mutations promote PCa progression by interacting with multiple cancer-specific pathways including β-catenin/LEF-1-mediated transcription and HIF-1α. Information presented in this dissertation demonstrates that ectopic [delta]-catenin gene is susceptible to mutagenesis when overexpressed in PCa cells, CWR22Rv-1 and PC-3, leading to sequence disruptions predicting functional alterations. It is shown that PCa cells overexpressing mutant [delta]-catenin increase β-catenin translocation to the nucleus and HIF-1α; expression when cultured under glucose deprived condition. These results suggest that [delta]-catenin mutations provide a survival advantage upon overgrowth and glucose deprivation over the control cells. Furthermore, we demonstrate that [delta]-catenin mutations promote tumor development in mouse prostate with probasin promoter (ARR₂PB)-driven, prostate specific expression of Myc oncogene. Additional investigations indicate that [delta]-catenin mutations in Myc transgenic mice not only promote β-catenin expression leading to dramatically elevated Myc expression but HIF-1α; is also increased in a [delta]-catenin gene-dosage dependent manner. Overall, we reveal that the introduction β-catenin mutations is an important step in metabolic adaptation by modulating β-catenin and HIF-1α; signaling in order to magnify its tumor promoting effect.;

949 a| Click on web addressw| ASISh| JOYNER101;

949 a| Click on web addressw| ASISh| HSL111;

949 o| jdjr;

994 a| C0b| ERE;

096 a| WJ 752;

596 a| 1 4;

998 a| 3486171;

999 a| CLICK ON WEB ADDRESSw| ASISc| 1i| 3486171-1001l| JNETm| JOYNERr| Ys| Yt| JNE3ETDu| 6/19/2014x| ETDz| JERESOURCE;

999 a| CLICK ON WEB ADDRESSw| ASISc| 1i| 3486171-2001l| HSLELECm| HSLr| Ys| Yt| HEETDu| 6/19/2014x| ETDz| HERESOURCE;

[Delta]-catenin: implications in prostate cancer progression / by Jongdee Nopparat.

Author/creator	Nopparat, Jongdee author.
Other author	Chen, Yan-Hua, degree supervisor.
Other author	East Carolina University. Department of Anatomy and Cell Biology.
Format	Theses and dissertations
Publication	[Greenville, N.C.] : [East Carolina University], 2014.
Description	218 pages : illustrations (some color)
Supplemental Content	Access via ScholarShip
Subjects	Prostatic Neoplasms--diagnosis. Catenins--metabolism. Adenocarcinoma--diagnosis.

Series	ECU Brody School of Medicine thesis ECU Brody School of Medicine thesis. ^A964744
General note	Presented to the faculty of the Department of Anatomy and Cell Biology.
General note	Advisor: Yan-Hua Chen.
General note	Title from PDF t.p. (viewed June 18, 2014).
General note	Non-Latin script record
Dissertation note	Ph.D. East Carolina University 2014.
Bibliography note	Includes bibliographical references.
Technical details	System requirements: Adobe Reader.
Technical details	Mode of access: World Wide Web.

Availability

Library	Location	Call Number	Status	Item Actions
	Electronic Resources	Access Content Online	✔ Available

[Delta]-catenin: implications in prostate cancer progression / by Jongdee Nopparat.

Click here for more information about this title

Availability