Aberrant expression and activation of receptor tyrosine kinases (RTK) is a frequent
feature of tumor cells that may underlie tumor aggressiveness. Among RTK, Axl, a
member of the Tyro3-Axl-Mer family, represents a potential therapeutic target in different
tumor types given its over-expression which leads to activation of oncogenic signaling promoting
cell proliferation and survival, as well as migration and invasion. Axl can promote aggressiveness of
various cell types through PI3K/Akt and/or MAPK/ERK, and its expression can be transcriptionally regulated
by multiple factors. Deregulated Axl expression and activation have been shown to be implicated in reduced
sensitivity of tumor cells to target-specific and conventional antitumor agents, but the precise mechanism underlying
these phenomena are still poorly understood. Several small molecules acting as Axl inhibitors have
been reported, and some of them are undergoing clinical investigation. In this review, we describe Axl biological
functions, its expression in cancer and in drug-resistant tumor cells and the development of inhibitors
tailored to this receptor tyrosine kinase.
Keywords: Cancer, receptor tyrosine kinases, Axl, drug resistance, invasion, inhibitors.
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