Biology & Sustainability
Assessment of Protein Expression Influenced by TAL1 in T-Cell Acute Lymphoblastic Leukemia
Document Type
Poster Presentation
Location
Indianapolis, IN
Subject Area
Biology & Sustainability
Start Date
11-4-2014 8:30 AM
End Date
11-4-2014 9:30 AM
Sponsor
James Olesen (Ball State University)
Description
The transcription factor, TAL1, is ectopically expressed in 60% of T-cell acute lymphoblastic leukemia (T-ALL) patients and may participate in poor chemotherapeutic response. TAL1 is thought to delay apoptosis by inhibiting the nuclear factor-kappa B (Nf-kB) pathway. Inhibition of the Nf-kB pathway allows for an atypical p65/c-Rel heterodimer to form, which may promote cellular proliferation. The correlation between TAL1 and transcriptional downstream targets of NF-kB is not fully characterized, however. Therefore, apoptosis was induced in the Jurkat T-cell line (model for T-ALL) through single and dual 24 hr drug treatments with etoposide and/or Tumor Necrosis Factor α (TNFα). Whole cell protein extractions were performed on control and drug-treated Jurkat cells and protein expression was assessed by Western blotting and flow cytometry. The proteins that were evaluated include: p65, c-Rel, cleaved caspase-8, TAL1, and β-tubulin. Normalized densitometric analysis of band intensity, corresponding to each protein, is currently being performed, as well as, the determination of normalized protein expression based on the flow data. Statistical analyses will then be performed to assess if there are expression differences in the aforementioned proteins. If differences in protein expression are evident, the role of TAL1 in the regulation of various proteins in Jurkat cells might be better understood. Potential therapeutic targets that inhibit the anti-apoptotic effects of TAL1 may thus be determined and lead to improved T-ALL treatment.
Assessment of Protein Expression Influenced by TAL1 in T-Cell Acute Lymphoblastic Leukemia
Indianapolis, IN
The transcription factor, TAL1, is ectopically expressed in 60% of T-cell acute lymphoblastic leukemia (T-ALL) patients and may participate in poor chemotherapeutic response. TAL1 is thought to delay apoptosis by inhibiting the nuclear factor-kappa B (Nf-kB) pathway. Inhibition of the Nf-kB pathway allows for an atypical p65/c-Rel heterodimer to form, which may promote cellular proliferation. The correlation between TAL1 and transcriptional downstream targets of NF-kB is not fully characterized, however. Therefore, apoptosis was induced in the Jurkat T-cell line (model for T-ALL) through single and dual 24 hr drug treatments with etoposide and/or Tumor Necrosis Factor α (TNFα). Whole cell protein extractions were performed on control and drug-treated Jurkat cells and protein expression was assessed by Western blotting and flow cytometry. The proteins that were evaluated include: p65, c-Rel, cleaved caspase-8, TAL1, and β-tubulin. Normalized densitometric analysis of band intensity, corresponding to each protein, is currently being performed, as well as, the determination of normalized protein expression based on the flow data. Statistical analyses will then be performed to assess if there are expression differences in the aforementioned proteins. If differences in protein expression are evident, the role of TAL1 in the regulation of various proteins in Jurkat cells might be better understood. Potential therapeutic targets that inhibit the anti-apoptotic effects of TAL1 may thus be determined and lead to improved T-ALL treatment.