Journal
CANCERS
Volume 8, Issue 11, Pages -Publisher
MDPI
DOI: 10.3390/cancers8110103
Keywords
AXL; GAS6; metastasis; cancer stem cell phenotype; immune suppression; therapy; proliferation; resistance; small molecule; decoy receptor
Categories
Funding
- NIH [CA-198291, CA-67166, CA-197713]
- Silicon Valley Foundation
- Sydney Frank Foundation
- Kimmelman Fund
- Department of Defense Ovarian Cancer Research Program [W81XWH-15-1-0097]
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The AXL receptor tyrosine kinase (AXL) has emerged as a promising therapeutic target for cancer therapy. Recent studies have revealed a central role of AXL signaling in tumor proliferation, survival, stem cell phenotype, metastasis, and resistance to cancer therapy. Moreover, AXL is expressed within cellular components of the tumor microenvironment where AXL signaling contributes to the immunosuppressive and protumorigenic phenotypes. A variety of AXL inhibitors have been developed and are efficacious in preclinical studies. These agents offer new opportunities for therapeutic intervention in the prevention and treatment of advanced disease. Here we review the literature that has illuminated the cellular and molecular mechanisms by which AXL signaling promotes tumor progression and we will discuss the therapeutic potential of AXL inhibition for cancer therapy.
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