癌基因是一类能诱导正常细胞产生癌变的基因。然而，当细胞抑癌机制正常时，癌基因的激活往往导致细胞衰老，阻止肿瘤发生。Ras是一个典型的癌基因，Ras诱导的细胞衰老（RIS）是当今衰老和癌症研究领域的一大热点。基于前期研究，我们提出：蛋白磷酸酶2A（PP2A）在RIS过程中起到了关键作用，抑制PP2A能促进Ras诱导的肿瘤的发生。本项目将全面检验PP2A在RIS过程中的作用，解析PP2A调节RIS的分子机制；研究临床上是否存在Ras与CIP2A（PP2A的抑制蛋白）同时激活的卵巢癌以及相关分子机制。本项目的顺利开展，将深化人们对RIS的认识，揭示PP2A介导的细胞衰老机制在预防肿瘤发生中的重要作用；研究CIP2A在Ras诱导的细胞衰老和肿瘤发生过程中的作用机制，不仅能有力地推动细胞衰老领域的研究，还能为以CIP2A和Ras信号通路为靶向的抗肿瘤药物的研发提供最新的理论基础和实验依据。

An oncogene is a gene that can actively transform normal cells and promote tumorigenesis. But on the contrary, when tumor suppressor mechanisms are normal in cells, activation of oncogenes can often induce cellular senescence and prevent tumorigenesis. Ras is a typical oncogene, and Ras-induced cellular senescence (RIS) is a key focus in the research field of aging and cancer. Based on our previous studies, we propose that protein phosphatase 2A (PP2A) plays a key role in RIS, and inhibition of PP2A facilitates tumorigenesis driven by Ras activation. In this project, we will comprehensively examine the roles of PP2A in the RIS processes and dissect the molecular mechanisms of PP2A to regulate RIS. In addition, we will search for the presence of ovarian cancer cases harboring co-activation of Ras and CIP2A (a suppressor of PP2A) and study the relevant molecular mechanisms. We hope this work will help deepen understanding of Ras-induced cell senescence for researchers and reveal the important roles of PP2A in mediating cellular senescence and preventing tumorigenesis. Studying the roles of CIP2A in the processes of Ras-induced senescence and tumorigenesis can not only strongly support the study of cellular senescence, but also provide the latest theoretical basis and experimental evidences for developing anticancer drugs targeting CIP2A and Ras signaling pathways.