c-Myc is a protein of the Myc family of transcription factors (c-Myc, B-Myc, L-Myc, N-Myc, and s-Myc) encoded by the MYC proto-oncogene. c-Myc was first discovered as the cellular homolog of the retroviral v-Myc oncogene. c-Myc is a transcription factor for genes involved in cell growth, proliferation, differentiation, and apoptosis. c-Myc contains a basic helix-loop-helix domain and a leucine zipper domain that allow for its heterodimerization with its binding partner Max. Myc/Max complexes are able to activate genes via the Myc transactivation domain (1). In healthy cells, c-Myc expression is tightly regulated by NFκB and other transcription control mechanisms. However, c-Myc translocations have been identified in numerous malignancies that allow deregulation and constitutive expression of c-Myc. c-Myc translocations account for almost 100% of Burkitt ’s lymphoma cases (2). Translocations and mutations in c-Myc account for up to one seventh of all U.S. cancer deaths. This discovery has led to extensive characterization of c-Myc with hopes of developing a novel targeted cancer therapeutic.
c-Myc has been studied for nearly 30 years. It has been implicated as a key oncogene in a number of different cancers. Pich et. al. used the c-Myc antibody to assess c-Myc expression in 50 patients with invasive ductal carcinoma, a form of male breast carcinoma (MBC) (3). The monoclonal c-Myc antibody was used to stain tissue samples and this expression data was combined with follow-up survival data. The group found that c-Myc overexpression significantly correlated with poor prognosis in MBC.
While transcriptional regulation of c-Myc has been fairly well characterized, Sanders et. al. sought to better understand the regulation of c-Myc at the protein level (4). This group used the liver as a natural system to study c-Myc during states of cellular quiescence and proliferation. First the group used the c-Myc antibody for immunoblotting to compare c-Myc levels in fetal and adult hepatocytes. Unexpectedly, c-Myc was found in equal abundance in the proliferative fetal cells as well as the quiescent adult cells. This led the group to use the c-Myc antibody to assess differences in localization between the two cell populations. Staining with the c-Myc antibody showed nucleolar sequestration in the quiescent adult cells. Meanwhile, distribution of c-Myc in fetal cells was dependent on the proliferative status of each cell. These data suggest that cellular localization of c-Myc is an important regulatory mechanism that could be breached in malignancies.
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