Development of new treatment for refractory malignant diseases and investigation of new cell death mechanisms

我们报道了沉积肽诱导的恶性横纹肌样细胞的自噬，发现AIF从线粒体向细胞核的易位与这种自噬有关。我们还分析了抑郁肽耐药细胞系的耐药机制，并在这些耐药细胞中激活了ERK通路。我们建立了易于肺转移的小鼠骨肉瘤细胞系，并用唑来膦酸和CPT11治疗。CPT11在体内抑制骨肉瘤细胞侵袭，抑制肺转移。我们还报道了BAALC外显子5作为儿童急性髓性白血病（AML）的一个新的不良预后因素和CEBPA突变作为一个良好的预后标志物。

We reported autophagy in malignant rhabdoid cells induced by depsipeptide and found that AIF translocation from mitochondria to nuclei has been related with this autophagy. We also analysed resistant mechanism of depsipeptide from our depsipepside-resisitant cell lines and ERK pathway was activated in these resistant cells. We established mouse osteosarcoma cell line which is easily metastasize to lung and treated those mice by zoledronic acid and CPT11. CPT11 inhibited invasion of osteosarcoma cells and inhibited lung metastasis in vivo. We also reported that exon 5 of BAALC as a new poor prognostic factor and CEBPA mutations as good prognostic marker in child acute myelogenous leukemia (AML).