One further newly published peer-reviewed article:

Tajima-Shirasaki et al. Eicosapentaenoic Acid Downregulates Expression
of the Selenoprotein P Gene by Inhibiting SREBP-1c Independently of the AMPK
Pathway in H4IIEC3 Hepatocytes. J Biol Chem. 2017 May 2. pii: jbc.M116.747006.

Introduction:

According to the purpose of the study, it was the aim to find out if hepatic SREBP1c induces the transcripition of SELENOP eicosapentaenoic acid (EPA)-dependently or rather if EPA, a polyunsaturated fatty acid (PUFA), inhibits the activity of SREBP1c.

Evaluation:

Without going into great detail, it is useful to consider the following three issues:

1. For knock-down experiments the authors used siRNA which simultaneously targets both, the SREBP1c and SREBP1a transcript (see here). What about SREBP1a?
2. In overexpression experiments the authors only transfected the precursor 1a isoform of SREBP1 but transfected separately both, the precursor AND mature isoform SREBP1c. (Only the mature SREBP1 protein is transcriptionally active). However, they have concluded: »The mature SREBP-1c overexpression especially inhibited the suppressive effect of EPA on SELENOP promoter activity (Fig. 3C); however, SREBP-1a overexpression had no effect (data not shown). These results suggest an association of SREBP-1c activity with the EPA-induced suppression of SELENOP expression.« What about the mature SREBP1a?
3. In regard to the ChIP assay they have used, the authors assume: »...treatment with EPA was found to decrease the binding of SREBP-1c to Selenop promoter (Fig.5B), indicating that EPA decreases SELENOP promoter activity and gene expression via SREBP-1c inactivation...« It is important to know that SREBPs function as dimers in which the individual molecules can form homo- or heteromers (see here). What about the mature SREBP1a?