Cs. Huang et al., SIGNAL-TRANSDUCTION THROUGH ATYPICAL PKCS, BUT NOT THE EGF RECEPTOR, IS NECESSARY FOR UVC-INDUCED AP-1 ACTIVATION IN IMMORTAL MURINE CELLS, Oncogene, 14(16), 1997, pp. 1945-1954
The exposure of mammalian cells to ultraviolet (u.v.) irradiation lead
s to activation of transcription factors, such as AP-1 and NF kappa B.
It is postulated that the EGF receptor but not protein kinase C (PKC)
is the major membrane mediator in UVC-induced signal transduction. We
demonstrate here that the antisense oligonucleotides of PKC zeta and
the dominant negative mutant of PKC lambda/iota as well as dominant ne
gative PKC zeta markedly blocked UVC-induced AP-1 activity. In contras
t, UVC-induced AP-1 activity in cells devoid of the EGF receptor (B82)
, is not significantly different from that of the stable transfectants
with a kinase-deficient EGF receptor (B82M721), or wild-type EGF rece
ptor (B82L). This was found at all UVC irradiation doses and time cour
ses studied, while high levels of EGF-induced AP-1 activity were obser
ved in B82L cells but not in B82 cells. This evidence strongly suggest
s that atypical PKCs, but not the EGF receptor, is necessary for UVC-i
nduced AP-1 activation in JB6 and B82 cells.