The regulation of selenoprotein P gene (SEPP1) expression is an active area of investigation with changes in SEPP1 noted under a broad spectrum of biological processes. In HepG2 cells and primary rat hepatocytes, promoter activity has been shown to be inhibited by cytokines including interleukin 1β, tumor necrosis factor α, interferon γ, and transforming growth factor β1 (Dreher et al. 1997; Mostert et al. 2001). This inhibition suggests that the SEPP1 gene product may function as a negative acute-phase protein in response to inflammation. Alternatively, promoter activity is stimulated in hepatic cells through the FOXO1a and HNF-4α transcription factors (Speckmann et al. 2008; Walter et al. 2008).
