Tal-1 is a transcription factor that is frequently ectopically expressed in the majority of cases of T-cell acute lymphoblastic leukemia (T-ALL). The ectopic expression of Tal-1 in patients with ALL has been found to decrease susceptibility to chemotherapeutic drugs and apoptosis. Thus, this study focuses on the effects of endogenously expressed Tal-1 in the Jurkat cell line on three Bcl-2 family members (Bcl-2, Bcl-xL, and Bid) and the inhibition of apoptosis and cell viability when exposed to apoptosis inducing drugs such as etoposide. The data obtained indicate that when treated with etoposide for 12 h Jurkat cells endogenously expressing Tal-1 have an 81% higher
level of anti-apoptotic Bcl-2 expression, an 18% lower level of anti-apoptotic Bcl-xL, expression, and a 31% lower level of pro-apoptotic Bid expression compared to Jurkat cells lacking Tal-1 expression.
The data also demonstrates that Jurkat cells endogenously expressing Tal-1 have a 15.94% lower amount of cell death after treatment with etoposide for 12 h and a 20.34% lower amount of cell death after treatment with etoposide for 24 h when compared to Jurkat cells that lack Tal-1 expression. Thus, the endogenous expression of Tal-1 increases the amount of the anti-apoptotic Bcl-2 expression and decreases the amount of the pro-apoptotic Bid creating an overall anti-apoptotic signal within the cell. / Department of Biology
| Identifer | oai:union.ndltd.org:BSU/oai:cardinalscholar.bsu.edu:123456789/193747 |
| Date | January 2008 |
| Creators | Wallace, Carrie T. |
| Contributors | Olesen, James B. |
| Source Sets | Ball State University |
| Detected Language | English |
| Format | ix, 101 p. : digital, PDF file, ill. (some col.). |
| Source | CardinalScholar 1.0 |
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