Satb1 promotes Schwann cell viability and migration via activation of PI3K/AKT pathway.

Abstract

Satb1 regulates chromatin structure and gene expression, and is aberrantly expressed in many tumors. However, there is still no report about Satb1 functions in peripheral nerve injury until now. In this study, we explored the regulatory effect of Satb1 on Schwann cells. MTT assay, transwell assay, and flow cytometry assay were respectively used to determine Schwann cell viability, migration, and apoptosis. The mRNA and phosphorylation levels of Satb1 and SHIP1 were assessed by RT-PCR and Western blotting analysis, respectively. The correlation between Satb1 and SHIP1 was examined by ChIP assay. The expressions of PI3K/AKT pathway related factors were detected by Western blotting. In the present study, we found that knock-out of Satb1 significantly inhibited cell viability and migration, and promoted Schwann cells apoptosis. Conversely, over-expression of Satb1 promoted cell viability, migration, and inhibited apoptosis. Satb1 inhibited SHIP1 expression by recruiting HDAC1. Furthermore, results showed that Satb1 activated the PI3K/AKT signaling pathway by inhibiting the expression of SHIP1. SHIP1 showed significant reversal effects on the regulatory roles of Satb1 in Schwann cells. Over-expression of Satb1 and SHIP1 inhibited cell viability, migration, and promoted apoptosis. Our study demonstrated that the Satb1 knock-out could inhibit the activation of PI3K/AKT pathway by up-regulating SHIP1, thus inhibiting cell viability and migration, and promoting Schwann cell apoptosis.