SIPL1 enhances the proliferation, attachment, and migration of CHO cells by inhibiting PTEN function

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...

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Bibliographic Details
Published in:International journal of molecular medicine 2014-09, Vol.34 (3), p.835-841
Main Authors: DE MELO, JASON, WU, VINCENT, HE, LIZHI, YAN, JUDY, TANG, DAMU
Format: Article
Language:English
Subjects:
AKT
Angiogenesis
Biotechnology
Cancer
Cell adhesion & migration
Cell growth
Cell proliferation
cell signalling
Gene expression
Genetic aspects
Genetic regulation
Immunoglobulins
Kinases
Lipids
Phosphatase
Physiological aspects
PI3 kinase
Plasmids
Proteins
PTEN
Rodents
Signal transduction
SIPL1
Studies
Tumor suppressor genes
Tumorigenesis
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Summary: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.
ISSN:1107-3756
1791-244X
DOI:10.3892/ijmm.2014.1840