导读：Bim(Bcl-2 interacting mediator of cell death)是新近发现的Bcl-2蛋白家族促凋亡成员之一。近期，光动力研究者发表论文称Bim参与了Photofrin介导的光动力反应诱导的细胞调亡，且认为增强Bim的活性可能成为抗肿瘤的一个潜在方向。
Photodynamic therapy (PDT) is a promising noninvasive technique, which has been successfully applied to the treatment of human cancers.Studies have shown that the Bcl-2 family proteins play important roles in PDT-induced apoptosis. However, whether Bcl-2-interacting mediator of cell death (Bim) is involved in photodynamic treatment remains unknown. In this study, we attempt to determine the effect of Bim on Photofrin photodynamic treatment (PPT)-induced apoptosis in human lung adenocarcinoma ASTC-a-1 cells.
The translocation of Bim/Bax of the cells were monitored by laser confocal scanning microscope. The levels of Bim protein and activated caspase-3 in cells were detected by western blot assay. Caspase-3 activities were measured by Caspase-3 Fluorogenic Substrate (Ac-DEVD-AFC) analysis. The induction of apoptosis was detected by Hoechst 33258 and PI staining as well as flow cytometry analysis. The effect of Bim on PPT-induced apoptosis was determined by RNAi.
BimL移位到线粒体响应PPT，与下游的促调亡蛋白Bax活化作用相似。PPT增加了细胞中Bim和激活的Caspase-3的水平并且通过RNA干扰技术降低Bim的表达从而大大的免受了Caspase-3的活性(干扰)。在shRNA-Bim 转染的细胞中PPT 诱导的细胞调亡被抑制了。
BimL translocated to mitochondria in response to PPT, similar to the downstream pro-apoptotic protein Bax activation. PPT increased the level of Bim and activated caspase-3 in cells and that knockdown of Bim by RNAi significantly protected against caspase-3 activity. PPT-induced apoptosis were suppressed in cells transfected with shRNA-Bim.
We demonstrated the involvement of Bim in PPT-induced apoptosis in human ASTC-a-1 lung adenocarcinoma cells and suggested that enhancing Bim activity might be a potential strategy for treating human cancers.
Cell Physiol Biochem. 2015;35(4):1527-36.
Involvement of Bim in Photofrin-mediated photodynamically induced apoptosis.
Wang X1, He X, Hu S, Sun A, Lu C.
1Laboratory of Neuronal Network and Brain Diseases Modulation, School of Medicine, Yangtze University, Jingzhou, China.