PLCD1 Suppresses Tumorigenesis - Therapeutic Strategies in Cancer Biology and Pathology - page 175

the activation of ERK1/2 proliferative signalling in MCF-7 cells. But MCF-7 cells
do express EGFR at low levels. Intriguingly they find that the PLCD1 effects on
growth are not reversible. This is possibly a consequence of other interacting factors,
such as DLC1 which is known to interact with PLCD1 which influences some cel-
lular features such as cell migration partly by an EGFR-MEK-dependent mechanism
(Shih et al., 2012). PLCD4 seems to play an important part in liver regeneration and
its disruption does interfere with cell proliferation. Possibly it co-operates with PKC
isoforms (Akutagawa et al., 2006). Many tissues do show differential expression
of PLC isoenzymes and also isoforms of PLCD itself. The differences in the mode
of action of PLCD1 and PLCD4 are still unclear. For all intents and purposes, the
PLCD isoforms have similar function, but they might differ with regard to membrane
targeting due to differences in membrane binding properties (Ananthanarayanan
et al., 2002) and these can quite conceivably translate into functional disparities and
distinctions.