GH fails to increase IGF1 expression in HepG2 cells

Levels of IGF1 mRNA were quantified using real-time qPCR and normalized to those of β-actin. (A) HepG2 cells were stimulated with increasing doses of GH for 18 hours. (B) HepG2 cells were treated with two independent sources of GH, recombinant (R) and purified (P) for 24 hours. (C) HepG2 cells were treated with 22.6 nM GH and histone deacetylase inhibitors, 10 mM Nicotinamide (N) or 1 μM Trichostatin A (T) for 6 hours. Regardless of incubation time, GH dose or transcriptional enhancement, GH-induction of IGF1 could not be verified, which is consistent with several datasets in the Gene Expression Omnibus database. (D) Gene Expression Omnibus data sets for experiments with primary human hepatocytes and the HepG2 cell line were mined for expression levels of growth hormone receptor (GHR), prolactin receptor (PRLR) and IGF1.