Aberrant cell cycle regulation in cervical carcinoma

Young Tae Kim, Min Zhao

Research output: Contribution to journalReview articlepeer-review

91 Citations (Scopus)


Carcinoma of the uterine cervix is one of the most common malignancies among women worldwide. Human papilloma-viruses (HPV) have been identified as the major etiological factor in cervical carcinogenesis. However, the time lag between HPV infection and the diagnosis of cancer indicates that multiple steps, as well as multiple factors, may be necessary for the development of cervical cancer. The development and progression of cervical carcinoma have been shown to be dependent on various genetic and epigenetic events, especially alterations in the cell cycle checkpoint machinery. In mammalian cells, control of the cell cycle is regulated by the activity of cyclin-dependent kinases (CDKs) and their essential activating coenzymes, the cyclins. Generally, CDKs, cyclins, and CDK inhibitors function within several pathways, including the P16INK4A-cyclin DI-CDK4/6-pRb-E2F, p21WAF1-p27KIP1-cyclinE-CDK2, and p14ARF-MDM2-p53 pathways. The results from several studies showed aberrant regulation of several cell cycle proteins, such as cyclin D, cyclin E, p16 INK4A, P21WAF1, and p27KIP1, as characteristic feature of HPV-infected and HPV E6/E7 oncogene-expressing cervical carcinomas and their precursors. These data suggested further that interactions of viral proteins with host cellular proteins, particularly cell cycle proteins, are involved in the activation or repression of cell cycle progression in cervical carcinogenesis.

Original languageEnglish
Pages (from-to)597-613
Number of pages17
JournalYonsei medical journal
Issue number5
Publication statusPublished - 2005 Oct

All Science Journal Classification (ASJC) codes

  • Medicine(all)


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