THs contribute to TCL malignant phenotype through angiogenesis induction. (A) Pearson correlation between ITGAV and ITGB3 with VEGFB and VEGFA levels in TCL patients. (B) mRNA levels of VEGFA and VEGFB in the panel of immature and mature TCLs after 24-hour treatment with TH-AG compared with CT. (C) Transcript abundance of VEGFA (right) and VEGFB (left) was evaluated in CUTLL1, HuT78, and OCI-Ly12 cell lines transfected for 48 hours with siRNA against ITGAV (si-ITGAV), ITGB3 (si-ITGB3), or noncoding sequence (si-CT) and then treated for 24 hours with TH-AG or agarose alone (as CT). (D) Transcript abundance of VEGFB (right) and VEGFA (left) was evaluated in CUTLL1, HuT78, and OCI-Ly12 cell lines after 24-hour treatment with 250 ng/mL vitronectin (VN). (E) Induction of HMEC1 cell migration by conditioned medium from CUTLL1 cells treated or not with TH-AG. Representative photographs (scale bar, 60 μm) of the endothelial cells that migrate through the chamber membrane in the presence of CT or conditioned medium. (F) Quantitation of HMEC1 cell migration by conditioned medium from CUTLL, HuT 78, and OCI-Ly12 cells treated or not with TH-AG and preincubated with the anti-VEGF bevacizumab (10 μg/mL) vs vehicle. (G) Cell migration quantitation of HMEC1 cells in the presence or absence of conditioned medium from si-RNA–transfected CUTLL1 cells treated with TH-AG vs CT for 24 hours. Mean ± SEM of at least 3 independent experiments are shown.