Fig 1.
Right. Axl signaling pathways and post-translational cleavage. Axl is a transmembrane receptor tyrosine kinase. Gas-6 ligand binding leads to dimerization and activation of cellular pathways including: epithelial-mesenchymal transition, survival, proliferation, angiogenesis, chemotherapy resistance, and immune suppression. left. Axl signaling pathways and post-translational cleavage. One mechanism to regulate Axl expression is cleavage of the extracellular domain by the sheddases ADAM10 and ADAM17. The cleavage product makes its way into the bloodstream as soluble Axl (sAxl).
Table 1.
Characteristics of the healthy control and glioblastoma (GBM) cohorts.
Fig 2.
The relationship between pre- and post-operative soluble Axl levels.
The blue closed circles represent patients with postoperative sAxl levels lower than their preoperative levels. The red open circles represent patients with postoperative sAxl levels higher than preoperative. The diagonal line denotes pre- and post-operative sAxl equality.
Fig 3.
The relationship between tumor volume metrics and soluble Axl levels.
Multiple scatter plots visualize the lack of correlation between tumor volume metrics and sAxl levels. The total tumor volume, necrotic tumor volume, and enhancing tumor volume were determined through volumetric analysis of preoperative MRI scans. The ratios of necrotic to total volume, enhancing to total volume, and necrotic to enhancing volume were then calculated.
Table 2.
Correlation between preoperative MRI tumor volume measurements and sAXL level.
Fig 4.
The expression of Axl and soluble Axl in patient derived glioblastoma cell lines.
(A) Axl protein expression as determined by Western blot. (B) Axl mRNA expression as determined by qRT-PCR. The mean value and standard deviations are plotted. Each measurement was performed in triplicate and the experiment repeated at least twice.
Table 3.
Axl expression and sAxl levels in patient derived glioblastoma cell lines.
Table 4.
Serum levels of soluble Axl in several cancers.