[Role of RCC1-mediated nuclear-cytoplasmic transport process in tumor initiation and progression and its potential clinical value].

In recent years, the social burden and medical pressure of malignant tumor treatment and prognosis have become increasingly heavy, and it is particularly urgent to decipher the molecular mechanism. The progression of malignant tumors is often closely related to abnormal cell cycle and abnormal nuclear-cytoplasmic distribution of key cycle proteins. Regulator of chromosome condensation 1 (RCC1), as a key molecule connecting the regulation of cell cycle and the regulation of nuclear-cytoplasmic transport process, has become a focus of research. RCC1, as the only known guanine nucleotide exchange factor of Ras-related nuclear protein (Ran), establishes and maintains the RanGTP concentration gradient on the chromosome surface by catalyzing the conversion of RanGDP to RanGTP, thus driving the nuclear-cytoplasmic transport of proteins and regulating the cell cycle process. Studies have shown that abnormal expression of RCC1 will destroy the nuclear-cytoplasmic distribution balance of key proteins such as p27Kip1 and S-phase kinase-associated protein 2 (Skp2), leading to the loss of control of the cell cycle and promoting tumorigenesis. This paper reviews the relationship between abnormal RCC1-mediated nuclear-cytoplasmic transport and the initiation and progression of tumors, and elaborates on the research progress of small molecule drugs, nucleic acid drugs and peptide inhibitors related to RCC1, providing new directions and ideas for the precise diagnosis and treatment of tumors and drug development.