Fig 1: Sunitinib-induced senescent ECs exhibited increased inflammatory chemokine secretion and attracted tumor cells (TCs) via chemokinesis. a HUVECs were treated with vehicle (0.1% DMSO) or sunitinib (20 µM) for 24 h, and the supernatant was collected and subjected to the cytokine array containing 25 inflammatory chemokines. b The staining densities of CCL6, C5a, chemerin, and IL-16 were presented relative to that of the control. The mean level in the control group was set to 1.0; n = 4. c HUVECs were treated with sunitinib (20 µM) or vehicle (0.1% DMSO) for 24 h, and the relative mRNA levels of CCL6, C5a, chemerin, and IL-16 were measured by real-time RT-PCR (n = 5). d, e 4T1 and MDA-MB-231 cells were cultured in the upper chamber, and HUVECs pre-treated with sunitinib (or vehicle) were cultured in the lower chamber. The number of cells that crossed the Transwell membrane toward the lower chamber was counted (n = 5). Data were presented as columns with mean ± SEM. f–i Blood samples from mice administrated with sunitinib (100 mg/kg) were harvested. The concentration of CCL6 (f), C5a (g), chemerin (h), and IL-16 (i) was determined by ELISA. Significance was assessed by unpaired t test with Welch’s correction