Targeting mrtl to Reverse Myc in Breast Oncogenesis
Abstract
Our lab has discovered a 15 kDa protein, designated mrtl (myc-related translation / localization regulatory factor), which is generated from the same mRNA as c-Myc. We found that mrtl may be capable of direct interaction with the c-myc mRNA, and that ectopic overexpression of mrtl is associated with loss of Myc from the nucleus. Based on these results, we hypothesized that: (a) mrtl may regulate Myc translation and localization to the nucleus; and (b) mrtl may be a significant contributor to Mycassociated breast oncogenesis. Our experimental approaches include expression of wild-type or mutant mrtl in cis to Myc, and assessment of the consequences for Myc translation. We are examining mrtl and Myc in a series of human breast surgical specimens ranging from non-malignant to primary breast tumors to metastatic lesions of breast tumor origin, and investigating how the Myc IRES and differential expression of the p64 and p67 isoforms may ultimately determine the malignant phenotype. The results are helping to elucidate the functional relationship between mrtl and Myc, and the involvement of mrtl in development and progression of human breast cancer.
Document Details
- Document Type
- Technical Report
- Publication Date
- Jun 01, 2011
- Accession Number
- ADA552553
Entities
People
- Scott Blume
Organizations
- University of Alabama