Medical School, Ningbo University, 315211, Ningbo, China.
Mol Biol Rep. 2010 Apr;37(4):1891-6. doi: 10.1007/s11033-009-9629-9. Epub 2009 Jul 21.
Our previous reports indicated that cyclic AMP response element-binding (CREB) protein was involved in the regulation of Bcl-2 expression in apoptotic HeLa cells induced by trichosanthin (TCS). Here we presented that blockade the binding site of CREB to Bcl-2 by a CRE decoy oligonucleotide abrogated the TCS-decreased Bcl-2 expression. Furthermore, overexpression of phosphorylated CREB (p-CREB) in cells transfected with p-CREB/GFP fusion construct resulted in an increase of Bcl-2 protein content, however, this increase was attenuated by TCS treatment. Therefore, this data supports the hypothesis that CREB is a possible upstream regulator of Bcl-2 in apoptotic HeLa cells induced by TCS. The study provides new insights into understanding the mechanism of TCS in the treatment of cervical cancer.
我们之前的报告表明,环磷酸腺苷反应元件结合蛋白(CREB)参与了天花粉蛋白(TCS)诱导的凋亡 HeLa 细胞中 Bcl-2 表达的调节。在这里,我们提出通过 CRE 诱饵寡核苷酸阻断 CREB 与 Bcl-2 的结合位点,可消除 TCS 降低 Bcl-2 表达的作用。此外,用 p-CREB/GFP 融合构建体转染的细胞中磷酸化 CREB(p-CREB)的过表达导致 Bcl-2 蛋白含量增加,但 TCS 处理会减弱这种增加。因此,这些数据支持 CREB 是 TCS 诱导的凋亡 HeLa 细胞中 Bcl-2 的上游调节因子的假说。该研究为理解 TCS 在宫颈癌治疗中的作用机制提供了新的见解。