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白细胞分化抗原13(cluster of differentiation 13,CD13)不仅能促进肿瘤细胞恶性发展,而且有助于肿瘤血管的生成。该研究下调骨肉瘤细胞(MG63)CD13表达,通过ELISA和Western blot观察骨肉瘤中CD13的表达对白细胞介素-6(interleukin-6,IL-6)释放和血管内皮细胞(vascular endothelial cell,HUVEC)中信号转导和转录激活子3酪氨酸705位点(signal transducer and activator of transcription~(Tyr705),STAT3~(Tyr705))磷酸化水平的影响。同时,检测MG63中CD13对HUVEC迁移、侵袭和血管管腔形成能力的调控作用和机制。结果显示,下调MG63中CD13表达可抑制IL-6释放,降低HUVEC中STAT3~(Tyr705)磷酸化水平,并抑制其迁移、侵袭和血管形成能力。而外源性IL-6能抵消下调MG63中CD13后对HUVEC的上述作用。因此,抑制骨肉瘤中CD13-IL-6-STAT3信号通路将阻止肿瘤血管形成,可成为骨肉瘤治疗的新靶点。
Cluster of differentiation 13 (CD13) can not only promote the malignant development of tumor cells, but also help tumor angiogenesis. This study downregulated the expression of CD13 in osteosarcoma cells (MG63). The expression of CD13 in osteosarcoma was detected by ELISA and Western blot. The effect of interleukin-6 (IL-6) release and vascular endothelial cell (HUVEC) ) Signal transduction and activator of transcription ~ (Tyr705), STAT3 ~ (Tyr705) phosphorylation level. At the same time, we examined the regulatory effect and mechanism of CD13 on the migration, invasion and angiogenesis of HUVEC in MG63. The results showed that down-regulation of CD13 expression in MG63 could inhibit the release of IL-6, decrease the phosphorylation of STAT3 Tyr705 in HUVEC, and inhibit its migration, invasion and angiogenesis. Exogenous IL-6 can counteract the above-mentioned effect on HUVEC after down-regulating CD13 in MG63. Therefore, the inhibition of CD13-IL-6-STAT3 signaling pathway in osteosarcoma will prevent tumor angiogenesis and become a new target for the treatment of osteosarcoma.