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035 a| (Sirsi) o891139851;

035 a| (OCoLC)891139851;

040 a| EREe| rdac| EREd| UtOrBLW;

049 a| EREE;

100 1 a| Nutter, Jennifer Makenzie,e| author.?| UNAUTHORIZED;

245 10 a| Interrelated role of Notch signaling and mTORC pathways in prostate cancer cell survival and growth /c| by Jennifer Makenzie Nutter.;

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

300 a| 51 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| 0.84Mb2| rda;

490 1 a| ECU Brody School of Medicine thesis;

538 a| System requirements: Adobe Reader.;

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

500 a| Presented to the faculty of the Department of Oncology.;

502 b| M.S.c| East Carolina Universityd| 2014.;

500 a| Advisor: Fred E. Bertrand.;

500 a| Title from PDF t.p. (viewed September 23, 2014).;

520 3 a| Prostate cancer is currently the second highest leading cause of cancer death in men. Notch is a transmembrane receptor protein that is part of a signaling pathway necessary in the normal development of the prostate. Notch1 signaling has been shown to be lost in prostate adenocarcinoma. One of prostate cancer's biggest risk factors is age and mTOR has been shown to be linked to longevity and age related diseases. mTOR exists as two complexes, mTORC 1/2, whose key functions are to control cell survival, metabolism, and growth. mTORC1/2 are often overexpressed in cancer. It was also reported that the mTORC1 pathway became inactivated when Notch1 signaling was inhibited in prostate cancer cell line PC-3. Herein, we suggest a link between Notch1 signaling and mTOR pathway activity which led to experiments with DU145 cells manipulated to have decreased Notch1 expression. The data shows that loss of Notch1 signaling causes decreased expression of the mTORC1 component Raptor as well as decreased phosphorylation of mTORC1 downstream target 4E-BP1 in conditions of cell stress. The mTORC2 pathway exhibited decreased phospho-mTOR (Ser2481) in normal conditions and decreased Rictor signaling in both normal and serum starved conditions when Notch1 expression was lost. The data also suggests there is less G[bata]L in conditions of stress in Notch1 knockdown cells. We hypothesize that downregulation of Notch1 signaling leads to the dysfunction of both mTOR pathways.;

504 a| Includes bibliographical references.;

650 2 a| Prostatic Neoplasmsx| chemistry.=| ^A944366;

650 2 a| Prostatic Neoplasmsx| pathology.=| ^A926035;

650 2 a| Adenocarcinoma.=| ^A924767;

650 2 a| TOR Serine-Threonine Kinases.=| ^A1205549;

650 2 a| Receptor, Notch1.=| ^A1260995;

653 a| Oncology;

700 1 a| Bertrand, Fred E.,e| degree supervisor.?| UNAUTHORIZED;

710 2 a| Brody School of Medicine.b| Office of Research and Graduate Studies.b| Biomedical Sciences. ?| UNAUTHORIZED;

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

856 40 z| Access via ScholarShipu| http://hdl.handle.net/10342/4564;

949 a| Click on web addressw| ASISh| JOYNER101o| jdjr;

949 a| Click on web addressw| ASISh| HSL111o| jdjr;

994 a| C0b| ERE;

096 a| WJ 762;

596 a| 1 4;

998 a| 3514289;

999 a| CLICK ON WEB ADDRESSw| ASISc| 1i| 3514289-1001l| JNETm| JOYNERr| Ys| Yt| JNE3ETDu| 9/23/2014x| ETDz| JERESOURCE;

999 a| CLICK ON WEB ADDRESSw| ASISc| 1i| 3514289-2001l| HSLELECm| HSLr| Ys| Yt| HEETDu| 9/23/2014x| ETDz| HERESOURCE;

Interrelated role of Notch signaling and mTORC pathways in prostate cancer cell survival and growth / by Jennifer Makenzie Nutter.

Author/creator	Nutter, Jennifer Makenzie author.
Other author	Bertrand, Fred E., degree supervisor.
Other author	Brody School of Medicine. Office of Research and Graduate Studies. Biomedical Sciences.
Format	Theses and dissertations
Publication	[Greenville, N.C.] : [East Carolina University], 2014.
Description	51 pages : illustrations (some color)
Supplemental Content	Access via ScholarShip
Subjects	Prostatic Neoplasms--chemistry. Prostatic Neoplasms--pathology. Adenocarcinoma. TOR Serine-Threonine Kinases. Receptor, Notch1.

Series	ECU Brody School of Medicine thesis ECU Brody School of Medicine thesis. ^A964744
Summary	Prostate cancer is currently the second highest leading cause of cancer death in men. Notch is a transmembrane receptor protein that is part of a signaling pathway necessary in the normal development of the prostate. Notch1 signaling has been shown to be lost in prostate adenocarcinoma. One of prostate cancer's biggest risk factors is age and mTOR has been shown to be linked to longevity and age related diseases. mTOR exists as two complexes, mTORC 1/2, whose key functions are to control cell survival, metabolism, and growth. mTORC1/2 are often overexpressed in cancer. It was also reported that the mTORC1 pathway became inactivated when Notch1 signaling was inhibited in prostate cancer cell line PC-3. Herein, we suggest a link between Notch1 signaling and mTOR pathway activity which led to experiments with DU145 cells manipulated to have decreased Notch1 expression. The data shows that loss of Notch1 signaling causes decreased expression of the mTORC1 component Raptor as well as decreased phosphorylation of mTORC1 downstream target 4E-BP1 in conditions of cell stress. The mTORC2 pathway exhibited decreased phospho-mTOR (Ser2481) in normal conditions and decreased Rictor signaling in both normal and serum starved conditions when Notch1 expression was lost. The data also suggests there is less G[bata]L in conditions of stress in Notch1 knockdown cells. We hypothesize that downregulation of Notch1 signaling leads to the dysfunction of both mTOR pathways.
General note	Presented to the faculty of the Department of Oncology.
General note	Advisor: Fred E. Bertrand.
General note	Title from PDF t.p. (viewed September 23, 2014).
Dissertation note	M.S. East Carolina University 2014.
Bibliography note	Includes bibliographical references.
Technical details	System requirements: Adobe Reader.
Technical details	Mode of access: World Wide Web.

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Interrelated role of Notch signaling and mTORC pathways in prostate cancer cell survival and growth / by Jennifer Makenzie Nutter.

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