Cfp. Lotfi et al., Role of ERK/MAP kinase in mitogenic interaction between ACTH and FGF2 in mouse Y1 adrenocortical tumor cells, ENDOCRINE R, 26(4), 2000, pp. 873-877
In G(0)/G(1) cell cycle-arrested Y1 adrenocortical cells FGF2 is a strong m
itogen, whereas ACTH(39) can be a weak mitogen or a strong anti-mitogenic a
gent. Phosphorylated ERK1/2-MAP kinases are undetectable by Western and imm
unocitochemistry assay in G(0)/G(1)-arrested Y1 adrenal cells. Cell entry i
nto S phase linearly correlates with migration of phosphorylated ERK to nuc
leus. FGF2 rapid and strongly triggers transient phosphorylation of ERK1/2,
whereas ACTH(39) is a poor ERK1/2 activator. But, the MEK1 inhibitor, PD98
059 (50 muM), inhibits cFos and cyclin D1 induction and DNA synthesis stimu
lation by both ACTH(39) and FGF2, suggesting that ERK1/2 activation mediate
s the strong and the weak mitogenic effect of, respectively, FGF2 and ACTH(
39). In addition, ACTH(39) antagonizes the FGF2 mitogenic effect keeping un
touched ERK1/2 activation, c-Fos and cyclin D1 induction.