Objective      To determine the role of scinderin (SCIN) in the regulation of self-renewal capacity of gastric cancer stem cells.       Methods      SCIN-knockdown gastric cancer cells

including gastric cancer cell line MGC803 and primary gastric cancer XN0422 cells

were established with SCIN specific shRNA (shSCIN). Colony and tumorsphere formation assays were used to estimate the effect of shSCIN on self-renewal capability of gastric cancer cells in vitro

and the xenograft assay in nude mice was employed to assess the effect of shSCIN on tumorigenecity of gastric cancer cells.       Results      The expression of SCIN was markedly higher in gastric cancer stem cells than gastric cancer cells. SCIN knockdown significantly decreased the capabilities of colony and tumorsphere formation in MGC803 and XN0422 cells. The colony number derived from SCIN knockdown and mock cells was 26.33±4.37 and 62.33±3.18 in MGC803 cells

and 14.67±3.38 and 49.67±2.19 in XN0422 cells

respectively. The number of tumorsphere formatted by SCIN knockdown and mock cells was 12.33±0.88 and 39.00±2.69 in MGC803 cells

and 15.67±1.76 and 33.33±1.65 in XN0422 cells (P0.01 for all)

respectively. Xenograft assay showed that the volume and weight of the tumor mass derived from SCIN-knockdown MGC803 and XN0422 cells were remarkably smaller/lighter than that of mock cells (P0.05 for all).       Conclusion      Silencing of SCIN can effectively inhibit the self-renewal of gastric cancer stem cells

suggesting that SCIN might be a promising target for gastric cancer therapy by targeting gastric cancer stem cells.