期刊
EUROPEAN JOURNAL OF CANCER
卷 50, 期 1, 页码 216-225出版社
ELSEVIER SCI LTD
DOI: 10.1016/j.ejca.2013.08.017
关键词
PTEN; Tumour suppressor; PI3K-Akt/PKB pathway; Non-genetic inactivation; Epigenetic, transcriptional, post-transcriptional and post-translational regulation; Cancer; Leukaemia
类别
资金
- Fundacao para a Ciencia e a Tecnologia (FCT), Portugal [PTDC/IC/83193/2007, PTDC/IC/83023/2007, PTDC/SAU-OBD/104816/2008, PTDC/SAU-ONC/113202/2009]
- FCT
- Fundação para a Ciência e a Tecnologia [PTDC/SAU-OBD/104816/2008, PTDC/SAU-ONC/113202/2009] Funding Source: FCT
Mutations and deletions of the tumour suppressor phosphatase and tensin homologue deleted on chromosome 10 (PTEN) are frequently involved in the development of cancer. However, PTEN is also tightly controlled by various non-genomic mechanisms. This review focuses on those mechanisms, namely on the epigenetic silencing of PTEN, post-transcriptional regulation by non-coding RNAs and post-translational modification. We summarise their involvement in cancer in general, and place some emphasis on leukaemia, where PTEN genetic lesions are relatively uncommon and, strikingly, high levels of PTEN expression frequently associate with PTEN functional inactivation. Overall, it is apparent that rather than looking strictly for PTEN genetic lesions and PTEN expression status, the key to evaluating the real impact of PTEN as a 'quasi-insufficient' tumour suppressor must rely on the complete understanding of PTEN's 'functional dose', incorporating the multiple layers of PTEN regulation in the cell that are ultimately compromised in a given cancer. (C) 2013 Elsevier Ltd. All rights reserved.
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