Salidroside, a natural active ingredient extracted from Rhodiola rosea, has been shown to exert antitumor activity against breast cancer Dong Young et al. [1Dong Young K.ang, Nipin S.p, Doh Hoon K.im, e al. Salidroside inhibits migration, invasion and angiogenesis of MDA‑MB 231 TNBC cells by regulating EGFR/Jak2/STAT3 signaling via MMP2[J] Int. J. Oncol. 2018 ;  53 : 877-885

Cliccare qui per andare alla sezione Riferimenti], colon cancer Sun et al. [2Sun Kuan-Xue, Xia Hong-Wei, Xia Rong-Long Anticancer effect of salidroside on colon cancer through inhibiting JAK2/STAT3 signaling pathway[J] Int. J. Exp. Pathol. 2015 ;  8 (1) : 615-621

Cliccare qui per andare alla sezione Riferimenti] and bladder cancer Tian et al. [3Tian L.i, Kewei X.u, Yifan L.iu. Anticancer effect of salidroside reduces viability through autophagy/PI3K/Akt and MMP‑9 signaling pathways in human bladder cancer cells[J] Oncol. Lett. 2018 ;  16 : 3162-3168

Cliccare qui per andare alla sezione Riferimenti]. However, the effect of salidroside on apoptosis and autophagy in gastric cancer remains unclear. In our research, we observed the biological effect of salidroside on human gastric cancer AGS cells. Our results demonstrated that salidroside inhibited the growth of AGS cells both in vivo and in vitro and exerted a proapoptotic effect on AGS cells as confirmed by flow cytometry, Hoechst staining and western blot analysis. Additionally, we found that salidroside decreased the phosphorylation of PI3K and Akt and that pretreatment with the PI3K/Akt agonist IGF-1 could weaken the proapoptotic effect of salidroside. Interestingly, the exposure of AGS cells to salidroside induced autophagy as indicated by transmission electron microscopy, mRFP-GFP-LC3 transfection and western blot analysis, suggesting that salidroside promoted autophagy in gastric cancer AGS cells. Furthermore, treatment with the autophagy inhibitor chloroquine enhanced salidroside-induced cell apoptosis, indicating that the autophagy mediated by salidroside may protect AGS cells from death. Additionally, we found that salidroside decreased the level of p-mTOR protein in a concentration-dependent manner and that pretreatment with IGF-1 decreased the expression of autophagy proteins, suggesting that salidroside induced autophagy through the PI3K/Akt/mTOR pathway. The above findings indicate that salidroside inhibited the growth of gastric cancer and induced apoptosis and protective autophagy through the PI3K/Akt/mTOR pathway. In summary, our study provides novel insights regarding the activity of salidroside against gastric cancer and contributes to the clinical application of salidroside combined with autophagy inhibitors as a chemotherapeutic strategy for human gastric cancer.