Abstract：
:Mutations in the parkin gene, which encodes a ubiquitin ligase, are a major genetic cause of parkinsonism. Interestingly, parkin also plays a role in cancer as a putative tumor suppressor, and the gene is frequently targeted by deletion and inactivation in human malignant tumors. Here, we investigated a potential tumor suppressor role for parkin in gliomas. We found that parkin expression was dramatically reduced in glioma cells. Restoration of parkin expression promoted G(1) phase cell-cycle arrest and mitigated the proliferation rate of glioma cells in vitro and in vivo. Notably, parkin-expressing glioma cells showed a reduction in levels of cyclin D1, but not cyclin E, and a selective downregulation of Akt serine-473 phosphorylation and VEGF receptor levels. In accordance, cells derived from a parkin-null mouse model exhibited increased levels of cyclin D1, VEGF receptor, and Akt phosphorylation, and divided significantly faster when compared with wild-type cells, with suppression of these changes following parkin reintroduction. Clinically, analysis of parkin pathway activation was predictive for the survival outcome of patients with glioma. Taken together, our study provides mechanistic insight into the tumor suppressor function of parkin in brain tumors and suggests that measurement of parkin pathway activation may be used clinically as a prognostic tool in patients with brain tumor.
journal_name
Cancer Resjournal_title
Cancer researchauthors
Yeo CW,Ng FS,Chai C,Tan JM,Koh GR,Chong YK,Koh LW,Foong CS,Sandanaraj E,Holbrook JD,Ang BT,Takahashi R,Tang C,Lim KLdoi
10.1158/0008-5472.CAN-11-3060subject
Has Abstractpub_date
2012-05-15 00:00:00pages
2543-53issue
10eissn
0008-5472issn
1538-7445pii
0008-5472.CAN-11-3060journal_volume
72pub_type
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