Melittin inhibits tumor angiogenesis modulated by endothelial progenitor cells associated with the SDF-1α/CXCR4 signaling pathway in a UMR-106 osteosarcoma xenograft mouse model

• DOI: 10.3892/mmr.2016.5215
• Publication Date: 2016-05-06T08:10:52Z
• Authors: GANG QIN; YONGQIANG CHEN; HAIDONG LI; SUYANG XU; YUMEI LI; JIAN SUN; WU RAO; CHAOWEI CHEN; MINDONG DU; KAIYI HE; YONG YE
• Keywords: Melittin

Endothelial progenitor cells (EPCs) are important in tumor angiogenesis. Stromal cell-derived factor-1α (SDF-1α) and its receptor C-X-C chemokine type 4 (CXCR4) key stem cell homing. Melittin, a component of bee venom, exerts antitumor activity, however, the underlying mechanisms remain to be elucidated. The present study aimed assess effects melittin on EPCs angiogenesis mouse model osteosarcoma. UMR‑106 were treated with various concentrations viability was determined using MTT assay. EPC adherence, migration tube forming ability assessed. Furthermore, SDF‑1α, AKT extracellular signal‑regulated kinase (ERK)1/2 expression levels detected by western blotting. Nude mice inoculated establish an osteosarcoma model. tumors injected melittin, assessed immunohistochemistry immunofluorescence. Melittin decreased EPCs. In addition, it adhesion, formation when compared control SDF‑1α‑treated cells. phosphorylated (p)‑AKT, p‑ERK1/2, SDF‑1α CXCR4 control. proportions cluster differentiation (CD)34/CD133 double‑positive 16.4±10.4% control, 7.0±4.4, 2.9±1.2 1.3±0.3% 160, 320 640 µg/kg per day, respectively (P<0.05). At 11 days, reduced size that (control, 4.8±1.3 cm3; 3.2±0.6, 2.6±0.5, 2.0±0.2 cm3 for µg/kg, respectively; all P<0.05). microvessel density, protein tumors. may decrease effect EPC‑mediated angiogenesis, possibly via inhibition SDF-1α/CXCR4 signaling pathway.