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ASAP2 (ArfGAP with SH3 domain, ankyrin repeat and PH domain 2; AMAP2)
is a multidomain ADP-ribosylation-factor GTPase-activating protein involved in
membrane trafficking, actin-cytoskeleton organization, focal-adhesion dynamics
and cell migration. In pancreatic ductal adenocarcinoma, ASAP2 can be amplified
and overexpressed, and high expression has been associated with poorer prognosis.
Experimental ASAP2 disruption reduced pancreatic-cancer-cell migration, supporting
a role in tumour invasion and metastasis. In hepatocellular carcinoma, elevated
ASAP2 promoted proliferation, migration, invasion, epithelial–mesenchymal
transition and lung metastasis, partly by sustaining HGF/c-MET signalling.
The typical cancer-associated direction is up, while the desired
anticancer modulation is down or functional inhibition.
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