Skip Navigation

Acta Biochimica et Biophysica Sinica 2009 41(2):97-107; doi:10.1093/abbs/gmn011
This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Google Scholar
Right arrow Articles by Fan, D.
Right arrow Articles by Zhang, H.
Right arrow Search for Related Content
PubMed
Right arrow Articles by Fan, D.
Right arrow Articles by Zhang, H.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© The Author 2009. Published by ABBS Editorial Office in association with Oxford University Press on behalf of the Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences.

The molecular mechanisms that underlie the tumor suppressor function of LKB1

Dahua Fan, Chao Ma and Haitao Zhang*

Department of Biochemistry and Molecular Biology, Guangdong Medical College, Zhanjiang 524023, China

* Correspondence address. Tel: +86-759-2388581; Fax: +86-759-2388994; E-mail: taohaizhang{at}tom.com


  Abstract

Germline mutations of the LKB1 tumor suppressor gene result in Peutz–Jeghers syndrome (PJS) characterized by intestinal hamartomas and increased incidence of epithelial cancers. Inactivating mutations in LKB1 have also been found in certain sporadic human cancers and with particularly high frequency in lung cancer. LKB1 has now been demonstrated to play a crucial role in pulmonary tumorigenesis, controlling initiation, differentiation, and metastasis. Recent evidences showed that LKB1 is a multitasking kinase, with great potential in orchestrating cell activity. Thus far, LKB1 has been found to play a role in cell polarity, energy metabolism, apoptosis, cell cycle arrest, and cell proliferation, all of which may require the tumor suppressor function of this kinase and/or its catalytic activity. This review focuses on remarkable recent findings concerning the molecular mechanism by which the LKB1 protein kinase operates as a tumor suppressor and discusses the rational treatment strategies to individuals suffering from PJS and other common disorders related to LKB1 signaling.

Keywords    LKB1; tumor suppressor; Peutz–Jeghers syndrome; lung adenocarcinoma

Received: September 1, 2008; Accepted: October 23, 2008
Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?




Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.