在细胞氧化应激过程中，诱导细胞早老或凋亡是抑制肿瘤发生的重要机制之一。转录因子HBP1是在细胞衰老和细胞凋亡过程中均发挥作用的双重活性的调控因子，但其作用机制不清。我们的研究初步证实HBP1是PIM1蛋白激酶的靶蛋白，PIM1可催化HBP1的磷酸化修饰，从而稳定HBP1蛋白的稳定性。HBP1还可以转录激活PIM1基因的表达，形成PIM1-HBP1-PIM1正反馈信号通路，进一步加强过氧化氢诱导的细胞凋亡和细胞早老过程。本研究将深入探讨PIM1-HBP1和HBP1-PIM1的调控机制，以及由此而形成的正反馈信号通路的作用机制、这条信号通路在细胞氧化应激过程中的作用。此研究将为探索衰老及肿瘤转化的本质提供理论与实验依据。

Premature senescence or apoptosis is a potential tumor-suppressive mechanism in cellular oxidative stress. Transcription factor.HBP1 is a dual factor in senescence and apoptosis, but the mechanism of its regulation is not clear. Our data tentatively demonstrated that HBP1 is a target of PIM1 protein kinase. PIM1 catalyzes phosphorylation of HBP1, thus enhancing HBP1 protein stability. Thereafter, HBP1 can transactivate the expression of PIM1 gene, forming a positive axis of PIM1-HBP1-PIM1 in signal transduction and strengthing cell apoptosis or premature senescence induced by hydrogen peroxide. In this study, we will explore thoroughly the regulation mechanisms of PIM1-HBP1 or HBP1-PIM1 and the positive axis of PIM1-HBP1-PIM1,as well as its roles in cell senescence and apoptosis. The investigation will provide theorial and experimental basis for exploring the characteristic essence of senescence and tumor transformation.