The
Adenosine diphosphate-Ribosylation Factor (ARF) family belongs to the RAS superfamily of
small GTPases and is involved in a wide variety of physiological processes, such as cell proliferation, motility and differentiation by regulating membrane traffic and associating with the cytoskeleton. Like other members of the RAS superfamily, ARF family
proteins are activated by
Guanine nucleotide Exchange Factors (GEFs) and inactivated by
GTPase-Activating Proteins (GAPs). When active, they bind effectors, which mediate downstream functions. Several studies have reported that
cancer cells are able to subvert membrane traffic regulators to enhance migration and invasion. Indeed, members of the ARF family, including ARF-Like (
ARL) proteins have been implicated in
tumorigenesis and progression of several types of
cancer. Here, we review the role of ARF family members, their GEFs/GAPs and effectors in
tumorigenesis and
cancer progression, highlighting the ones that can have a pro-oncogenic behavior or function as
tumor suppressors. Moreover, we propose possible mechanisms and approaches to target these
proteins, toward the development of novel therapeutic strategies to impair
tumor progression.