抑癌因子RBM38在前列腺癌发生发展中的分子机制研究

Prostate cancer (PCa) is one of the most prevalent cancers affecting men in the world. The major therapy for patients with advanced PCa is androgen deprivation therapy (ADT). But in most cases, patients will become drug-resistant and ultimately fail treatment. Therefore, exploration of new therapeutic targets has been a key focus in malignant PCa research. Our research group has found that RBM38, an RNA-binding protein with splicing regulatory functions, may have the potential to inhibit global RNA splicing, consequently impeding the initiation and progression of PCa. However, the specific role of RBM38 in PCa remains unexplored, and the underlying molecular mechanisms are not yet clearly defined. Hence, this study intends to explore the role and molecular mechanism of RBM38 in prostate tumorigenesis. According to bioinformatical analysis, the expression of RBM38 is down-regulated in PCa(vs. normal) tissues and positively correlated with favorable prognosis of patients. Meanwhile, RBM38 is potentially associated with many key cancer-related pathways. We show that RBM38 overexpression can inhibit the malignant biological properties of PCa cells by phenotypic experiments. Mechanically, analyses of RNA-seq and proteomic have revealed that RBM38 overexpression can promote immune-related gene expression, inhibit global RNA splicing andtranslation. Altogether, this study demonstrates that RBM38 functions as a tumor suppressor in PCa, which may yeild new ideas for the diagnosis and treatment of aggressive PCa.