• The inhibition of Panc1 cancer cells invasion by hAMSCs secretome through suppression of tyrosine phosphorylation of SGK223 (at Y411 site), c‑Src (at Y416, Y530 sites), AKT activity, and JAK1/Stat3 signaling
  • Nasim Shafiee Nejad,1 Fatemeh Safari,2,*
    1. University of Guilan - Faculty of Sciences
    2. University of Guilan - Faculty of Sciences


  • Introduction: SGK223 is a scaffolding protein involving in the oncogenic tyrosine kinase signaling. SGK223 was phosphorylated at Y411 by c-Src and in response to the Epidermal growth factor receptor (EGFR). Tyrosine phosphorylated SGK223 at Y411 enables to interact with CSK resulting up regulation of c-Src activity and promotion of the cell migration. Human amniotic mesenchymal stromal cells (hAMSCs) are a population of multipotent cells that it was considered to be as a potential platform in cancer therapy.
  • Methods: Herein, we employed a co-culture system to clarify the effects of hAMSCs secretome through tyrosine phosphorylation of c-Src, SGK223, AKT activity, and JAK1/Stat3 signaling in Panc1 pancreatic cancer cells. By using the 0.4 μm pore sized transwell membranes, both cell lines were firstly co-cultured for 72 h. Next, c-Src activity (tyrosine phosphorylation levels at Y530 and Y416), tyrosine phosphorylation level of SGK223 (at Y411), AKT activity, and JAK1/Stat3 signaling in Panc1 cells after treatment with hAMSCs were evaluated.
  • Results: Our results showed that hAMSCs have the inhibitory effects on Panc1 pancreatic cancer cells invasion.
  • Conclusion: It suggests that the suppression of c-Src activity, SGK223 expression, AKT activity, and JAK1/Stat3 signaling may be as critical targets in pancreatic cancer therapy.
  • Keywords: Stem cells, pancreatic cancer cells, AKT, SGK223, JAK1/Stat3 signaling