The PI3K/Akt pathway plays a vital role in cell survival by suppressing apoptosis and promoting cell proliferation (Vivanco and Sawyers, 2002). Akt, an essential serine/threonine kinase, is a crucial component of the PI3K signaling pathway, and its activation has been involved in the genesis or progression of many human malignancies (Blume-Jensen and Hunter, 2001; Vivanco and Sawyers, 2002). Previous studies showed that AKT1 and AKT2, the target genes of PI3K, are overexpressed in breast, gastric and ovarian cancers (Staal, 1987; Bellacosa et al., 1995). Many studies demonstrated that the constitutively active PI3K or Akt is oncogenic in cell systems and animal tumor models (Chang et al., 2003; Liu et al., 2015). Several studies have shown that Akt/PKB is involved in immune activation, cell proliferation, apoptosis and cell survival through activating the transcription of a variety of genes (Fowles et al., 2015; Warfel and Kraft, 2015). Our study revealed that significant upregulation of GSN inhibited the PI3K/Akt pathway in YTS cells. A previous study revealed that the cytoskeletal protein GSN was a vital determinant of cell invasion and scattering by inhibiting E-cadherin expression through the HGF-PI3K-Akt signaling pathway in gastric cancer (Huang et al., 2016). In addition, it has been reported that constitutive PI3K/Akt activation promotes the progress of prostate cancer from an organ-conﬁned disease to a highly invasive and even possibly metastatic disease. Due to its role as a vital regulator of cell survival, Akt has been considered as a crucial factor in tumorigenesis (Nowinski et al., 2015). Consistent with that, in our study, blocking the PI3K/Akt pathway inhibited cell proliferation and invasion of YTS cells, while promoting apoptosis.