Loss-of-parkin function enhances cyclin D1 expression and AKT signalling and promotes glioblastoma cell proliferation

ABSTRACT: Mutations in the parkin gene, which encodes a ubiquitin ligase, are a major cause of autosomal recessive parkinsonism. Interestingly, parkin also plays a role in cancer as a putative tumor suppressor. Consistent with this, the gene is frequently targeted by deletion and inactivation in human malignant tumors. Here, we show that parkin expression is dramatically reduced in glioma cells, which correlates with increased cancer mortality. We further show that restoration of parkin expression in these cells promotes their arrest at G1 phase and significantly mitigates their proliferation rate both in vitro and in vivo. Notably, the level of cyclin D1, but not cyclin E, is reduced in parkin-expressing glioma cells. Moreover, parkin expression also leads to a selective downregulation of Akt serin

ORGANISM(S): Homo sapiens

SUBMITTER: Felicia Ng 

PROVIDER: E-GEOD-29494 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress