The proliferation of tumor cells is regulated by a complex array of signaling pathways, among these signaling pathways,the programmed cell death. Autophagy and apoptosis are two types of programmed death. There are significant differences in their morphological and functional features, but they also have many links. Both apoptosis and autophagy are involved in activation,expression and regulation of a series of genes. By reviewing the research progress in recent years, this article will discuss the cellular regulation and molecular mechanisms of their related genes. Through summarizing the relationship between autophagy and apoptosis,it aims to get a better understanding of the mechanisms of autophagy and apoptosis in tumor progression,and looking at the perspectives for studies on the autophagy and apoptosis in tumor treatment.

ObjectiveTo explore the mechanism of Si Junzitang in regulating the expression of NKG2A to affect the anti-colon cancer function of natural killer （NK） cells. MethodNK cells isolated from healthy honors were cultured and used to construct the three incubation models of NK cells， human colon cancer HCT116 cells， and NK cells + HCT116 cells （co-incubation）. real-time fluorescence quantitative polymerase chain reaction （Real-time PCR） was conducted to determine the mRNA levels of natural killer group 2 member A （NKG2A） and interleukin （IL）-15 in NK cells， as well as the mRNA level of histocompatibility leucocyte antigen E （HLA-E） in HCT116 cells. The secretion of IL-15 was detected by enzyme-linked immunosorbent assay （ELISA）. Methyl thiazolyl tetrazolium （MTT） assay was employed to determine the applicable concentration of IL-15 and test the effects of Si Junzitang and IL-15 on the activities of NK cells and the HCT116 cells in the co-incubation model. The effects of Si Junzitang and IL-15 on the mRNA levels of NKG2A in NK cells and HLA-E in HCT116 cells were detected by Real-time PCR. Monalizumab （M， anti-NKG2A mab） was used to block the NKG2A-HLA-E pathway in co-incubation model， and then the proliferation of HCT116 cells was detected by MTT assay. ResultThe interaction of NK cells and HCT116 cells up-regulated the mRNA levels of NKG2A in NK cells and HLA-E in HCT116 cells （P<0.05）， as well as the expression level and secretion of IL-15 （P<0.05）. Compared with the blank group， Si Junzitang and Si Junzitang + IL-15 promoted the proliferation and improved the anti-colon cancer function of NK cells （P<0.01）. Furthermore， they down-regulated the mRNA levels of NKG2A in NK cells and HLA-E in the HCT116 cells co-incubated with NK cells （P<0.01）. M and IL-15 + M inhibited the proliferation of HCT116 cells compared with the groups without M （P<0.01）. ConclusionThe interaction of NK cells and HCT116 cells can induce activation of NKG2A-HLA-E pathway to impair NK cell function. Si Junzitang can inhibit the activation of NKG2A-HLA-E pathway to restore the anti-colon cancer function of NK cells.