Caspase Deficiency: Involvement in Breast Carcinogenesis and Resistance
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.
Document Details
- Document Type
- Technical Report
- Publication Date
- Jul 01, 2003
- Accession Number
- ADA420325
Entities
People
- Xiaohe Yang
Organizations
- University of Oklahoma Health Sciences Center