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003 OCoLC;

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008 041013s2003 xx a bm 000 0 eng d;

035 a| (Sirsi) o56722045;

035 a| (OCoLC)56722045;

049 a| EREE;

050 4 a| QH671b| .B45 2003;

100 1 a| Bell, Charles W.,e| author.=| ^A584584;

245 10 a| Characterization of MCF-10A/BCL-2 cells /c| by Charles W. Bell.;

264 0 c| 2003.;

300 a| vii, 100 leaves :b| illustrations (some color) ;c| 28 cm;

336 a| textb| txt2| rdacontent;

337 a| unmediatedb| n2| rdamedia;

338 a| volumeb| nc2| rdacarrier;

502 b| M.S.c| East Carolina Universityd| 2003;

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

500 a| Advisor: Mary Farwell;

520 3 a| Bcl-2 is the prototypical member of the Bcl-2 family of proteins that are involved in apoptosis. It has been shown to be over expressed in many cancer cells. Bcl-2 has been localized to the mitochondria, ER, and nucleus, and when localized to the mitochondria Bcl-2 has shown to prevent apoptosis. Bcl-2 has been shown to slow the proliferation of cells, delay them in Gj/Go of the cell eycle, and increase the mitochondrial membrane potential, ATm- Previously, MCE-10A, an immortalized human mammary epithelial cell line, was induced to overexpress Bcl-2, resulting in the MCF-lOA/Bel-2 cell line. The MCF-lOA/Bcl-2 cells have been shown to have a slower proliferation rate compared to the control cells. We hypothesized that the MCF-IOA/Bcl2 cells would be delayed in Gi/Go compared to control cells, MCF-IOA/Neo cells (cells containing neomycin resistant marker alone). Cell cycle analysis was carried out by two methods. In the first, cells were synchronized by removal of growth factors (GF) for 5 days and then GF were added back. This experiment showed that the MCF-lOA/Bcl-2 cells were delayed in Gq/Gi of the cell cycle. The second method for cell cycle analysis was colchicine treatment of cells for 5 days. These results showed the MCF-lOA/Bcl-2 cells were delayed in Gq/Gi of the cell cycle. MCF-lOA/Bcl-2 cells appeared to die at a greater rate than the MCF-IOA/Neo cells when treated with colchicine by the amount of sub-Gi debris. Analysis by acridine orange and ethidium bromide staining showed that the MCF-lOA/Bcl-2 cells delay apoptosis when treated with colchicine however, the cells died at a faster rate later in the experiment compared to MCF-IOA/Neo cells.;

504 a| Includes bibliographical references (leaves 58-68).;

650 0 a| Apoptosis.=| ^A294849;

650 0 a| Cell cyclex| Analysis.=| ^A4972;

650 0 a| Colchicine.=| ^A321854;

650 2 a| Apoptosis0| (DNLM)D017209=| ^A929574;

650 2 a| Colchicine0| (DNLM)D003078=| ^A1462492;

655 2 a| Academic Dissertation.0| (DNLM)D019478?| UNAUTHORIZED;

650 7 a| Apoptosis.2| fast0| (OCoLC)fst00811467;

650 7 a| Colchicine.2| fast0| (OCoLC)fst00866953;

655 7 a| Academic theses.2| fast0| (OCoLC)fst01726453;

655 7 a| Academic theses.2| lcgft;

655 7 a| Thèses et écrits académiques.2| rvmgf0| (CaQQLa)RVMGF-000001173;

700 1 a| Farwell, Mary A.,e| degree supervisor.?| UNAUTHORIZED;

710 2 a| East Carolina University.b| Department of Biology.=| ^A637467;

856 41 z| Access via ScholarShipu| http://hdl.handle.net/10342/11860;

949 a| Click on web addressw| asish| joyner101;

949 a| Click on web addressw| asish| hsl111;

994 a| C0b| ERE;

998 a| 974654;

596 a| 1 4;

999 a| ASK AT SPECIAL COLLECTIONS DESKw| ASISc| 1i| MQ1723616l| JSCJTHDm| JOYNERr| Ys| Yt| JSCJTHDu| 10/14/2004x| ETDz| JSPECCOLLo| .STAFF. 0;

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Characterization of MCF-10A/BCL-2 cells / by Charles W. Bell.

Author/creator	Bell, Charles W. author.
Other author	Farwell, Mary A., degree supervisor.
Other author	East Carolina University. Department of Biology.
Format	Theses and dissertations
Production	2003.
Description	vii, 100 leaves : illustrations (some color) ; 28 cm
Supplemental Content	Access via ScholarShip
Subjects	Apoptosis. Cell cycle--Analysis. Colchicine. Apoptosis Colchicine

Summary	Bcl-2 is the prototypical member of the Bcl-2 family of proteins that are involved in apoptosis. It has been shown to be over expressed in many cancer cells. Bcl-2 has been localized to the mitochondria, ER, and nucleus, and when localized to the mitochondria Bcl-2 has shown to prevent apoptosis. Bcl-2 has been shown to slow the proliferation of cells, delay them in Gj/Go of the cell eycle, and increase the mitochondrial membrane potential, ATm- Previously, MCE-10A, an immortalized human mammary epithelial cell line, was induced to overexpress Bcl-2, resulting in the MCF-lOA/Bel-2 cell line. The MCF-lOA/Bcl-2 cells have been shown to have a slower proliferation rate compared to the control cells. We hypothesized that the MCF-IOA/Bcl2 cells would be delayed in Gi/Go compared to control cells, MCF-IOA/Neo cells (cells containing neomycin resistant marker alone). Cell cycle analysis was carried out by two methods. In the first, cells were synchronized by removal of growth factors (GF) for 5 days and then GF were added back. This experiment showed that the MCF-lOA/Bcl-2 cells were delayed in Gq/Gi of the cell cycle. The second method for cell cycle analysis was colchicine treatment of cells for 5 days. These results showed the MCF-lOA/Bcl-2 cells were delayed in Gq/Gi of the cell cycle. MCF-lOA/Bcl-2 cells appeared to die at a greater rate than the MCF-IOA/Neo cells when treated with colchicine by the amount of sub-Gi debris. Analysis by acridine orange and ethidium bromide staining showed that the MCF-lOA/Bcl-2 cells delay apoptosis when treated with colchicine however, the cells died at a faster rate later in the experiment compared to MCF-IOA/Neo cells.
General note	Presented to the faculty of the Department of Biology.
General note	Advisor: Mary Farwell
Dissertation note	M.S. East Carolina University 2003
Bibliography note	Includes bibliographical references (leaves 58-68).
Genre/form	Academic theses.
Genre/form	Academic theses.
Genre/form	Thèses et écrits académiques.

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