TGF-β1、TβRⅡ、c-myc在急性白血病中的表达及其意义

为了探讨转化生长因子β（transforming growth factor—beta，TGF-β）信号转导途径失活与急性白血病的关系，用S—P免疫细胞化学法检测急性白血病患者骨髓单个核细胞中TGF—β1及其Ⅱ型受体（TβRⅡ）和信号下游靶基因蛋白C-myc的表达。结果发现，白血病患者骨髓单个核细胞中TGF—β1的表达水平与正常对照无显著性差异（P〉0．05），TβRⅡ的表达水平明显低于正常对照（P〈0．05），c-myc的表达水平明显高于正常对照（P〈0．05），但以上各指标在急性淋巴细胞白血病与急性非淋巴细胞白血病之间无显著性差异（P〉0．05），TβRⅡ和c-myc表达率有负相关关系（r=-0．474，P〈0．01）。结论：TGF-β信号转导途径失活使细胞逃逸了TGF-β的生长抑制，TGF-β信号转导途径失活的一个重要机制就是通过TGF-βⅡ型受体的下调使c-myc失去抑制而高表达，促进白血病发生。

Expression and Significance of TGF-β1 、TβR Ⅱ and c-myc in Patients with Acute Leukemia

To explore the relationship between inactivation of TGF-beta signaling pathway and acute leukemia, the expressions of TGF-beta1, TbetaRII and c-myc in the bone marrow mononuclear cells were detected by S-P immunocytochemical staining. The results showed that no significant difference of TGF-beta1 exepression was found between the patients and the control (P > 0.05), the expression of TbetaRII was significantly lower in patients than in control (P < 0.05) and the expression of c-myc was significantly higher in patients than in control (P < 0.05). There was no significant difference of TGF-beta1, TbetaRII and c-myc exepression between acute nonlymphoid leukemia and acute lymphoid leukemia (P > 0.05). Expressions of TbetaRII and c-myc were negatively correlated (r = -0.474, P < 0.01). In conclusion, the leukemic cells escape from the growth inhibitory effect because of the inactivation of TGF-beta signaling pathway; downregulation of TGF-beta receptor II cause c-myc overexepression and leukemogenesis.