期刊
MEDICAL MICROBIOLOGY AND IMMUNOLOGY
卷 208, 期 5, 页码 573-583出版社
SPRINGER
DOI: 10.1007/s00430-018-0570-1
关键词
Epstein-Barr virus (EBV); Neoplasm; Cell cycle; Molecular mechanism
资金
- National Natural Science Foundation of China [81372134, 81641012]
- Hunan Province Key Laboratory of Tumor Cellular and Molecular Pathology [2016TP1015]
- Hunan Province Cooperative Innovation Center for Molecular Target New Drug Study [2014-405]
The early stage of oncogenesis is linked to the disorder of the cell cycle. Abnormal gene expression often leads to cell cycle disorders, resulting in malignant transformation of human cells. Epstein-Barr virus (EBV) is associated with a diverse range of human neoplasms, such as malignant lymphoma, nasopharyngeal carcinoma and gastric cancer. EBV mainly infects human lymphocytes and oropharyngeal epithelial cells. EBV is latent in lymphocytes for a long period of time, is detached from the cytoplasm by circular DNA, and can integrate into the chromosome of cells. EBV expresses a variety of latent genes during latent infection. The interaction between EBV latent genes and oncogenes leads to host cell cycle disturbances, including the promotion of G(1)/S phase transition and inhibition of cell apoptosis, thereby promoting the development of EBV-associated neoplasms. Molecular mechanisms of EBV-driven cell cycle progression and oncogenesis involve diverse genes and signal pathways. Here, we review the molecular mechanisms of EBV-driven cell cycle progression and promoting oncogenesis.
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