Journal
INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE
Volume 34, Issue 3, Pages 835-841Publisher
SPANDIDOS PUBL LTD
DOI: 10.3892/ijmm.2014.1840
Keywords
SIPL1; PTEN; cell signalling; PI3 kinase; AKT
Categories
Funding
- Canadian Institute of Health Research (CIHR) [COP-107971]
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The PTEN tumour suppressor plays critical roles in inhibiting cell proliferation, adhesion and migration through downregulation of the PI3K-AKT pathway. SIPL1 is a novel PTEN-negative regulator (PTEN-NR) that contributes to PTEN inactivation during tumorigenesis. However, whether SIPL1 plays a role in inhibiting PTEN function in the process of cell adhesion and migration remains unclear. The aim of this study was to investigate this possibility using CHO-K1 cells, and western blotting, qPCR analyses and microscopy. Results showed that the overexpression of SIPL1 in CHO-K1 cells decreased the amount of PTEN protein. The downregulation was not caused by an obvious reduction in PTEN mRNA levels or ubiquitin-dependent protein degradation. Nonetheless, the reduction was functional, as SIPL1 overexpression increased the activation of AKT under serum-starved conditions, promoting CHO-K1 cell proliferation in an AKT-dependent manner. Furthermore, SIPL1 increased the migration and attachment of CHO-K1 cells. Taken together, the evidence suggested that SIPL1 promotes AKT activation by decreasing the amount of PTEN protein in CHO-K1 cells, thereby promoting cell proliferation and migration.
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