Accession Number : ADA420325
Title : Caspase Deficiency: Involvement in Breast Carcinogenesis and Resistance
Descriptive Note : Annual rept. 1 Jul 2002-30 Jun 2003
Corporate Author : OKLAHOMA UNIV HEALTH SCIENCES CENTER OKLAHOMA CITY
Personal Author(s) : Yang, Xiaohe
Report Date : JUL 2003
Pagination or Media Count : 30
Abstract : In the past year, our work focused on defining the functional impact of specific caspase deficiency as proposed in aim 3. We demonstrated that caspase-3 had feedback action on cytochrome c release in TNF-(L treated cells, as it was observed in doxorubicin treated cells. We also found that functional caspase 3 contributed to the up regulation of Fas in the cells treated with chemotherapeutic agents. To study the interactions between caspase- 3 and bcl-2, we have established bcl-2 overexpression cell lines with or without caspase-3 expression, and found that high levels of caspase-3 and bcl-2 were not compatible. To study the specific role of caspase-3 and p53 dependent apoptosis, using SiRNA technology, we have established p53 knock out cell lines form MCF-7/pv, MCF-7/caspase 3 and MDA-MB-23l cells. We also studied the role of caspase 10 in chemotherapy responsiveness by examining the sensitivity of control and caspase-lO reconstituted MCF-7 cells to doxorubicin and etoposide. With our collaborators, we studied down regulation of caspase-3 in human breast cancers. The results and the cell lines generated in last year will facilitate the accomplishment of the proposed project.
Descriptors : *BREAST CANCER, IMPACT, HUMANS, SENSITIVITY, FEEDBACK, DEFICIENCIES, THERAPY, RESPONSE(BIOLOGY), CELLS(BIOLOGY), CHEMOTHERAPY, MAMMARY GLANDS, BLOOD PROTEINS, CHEMOTHERAPEUTIC AGENTS, COLLABORATIVE TECHNIQUES, ONCOGENESIS.
Subject Categories : ANATOMY AND PHYSIOLOGY
MEDICINE AND MEDICAL RESEARCH
Distribution Statement : APPROVED FOR PUBLIC RELEASE