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

Abstract

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.