Objective      To determine the role of scinderin (SCIN) in regulating proliferation of gastrointestinal stromal tumor (GIST) cells.       Methods      SCIN-knockdown GIST cells were established with SCIN-specific shRNAs (shSCINs). The knockdown efficiency was determined by Western blotting and qRT-PCR. CCK-8 assay was used to evaluate imatinib IC50 and the effect of shSCIN on proliferation. Plate colony formation assay was used to test the effect of shSCINs on colony formation of GIST cells. Xenograft assay in nude mice was employed to test the effect of shSCINs on tumor growth. According to different treatment

GIST cells were divided into 4 groups: wild type group (WT group

no transfection)

mock group (transfected with scrambled siRNA)

shSCIN1 group (transfected with shSCIN1) and shSCIN 2 group (transfected with shSCIN2).       Results      The cell proliferation of shSCIN1 group and shSCIN2 group was significantly decreased compared with the mock group. The proliferation difference was significant from the second day to the seventh day (n=4

P0.05). Xenografts derived from shSCIN1 cells had significantly lower tumor weight than those derived from mock cells (0.1750±0.0456 vs 0.3341±0.0165 g

n=4

P0.01). The colony numbers derived from shSCIN1 cells and mock cells were 59.67±5.68 and 123.33±2.52

respectively (n=3

P0.01). After treatment with 0.57 μmol/L imatinib in WT cells for 1

3 and 5 d

the expression of SCIN was found to be decreased in a time-dependent manner.       Conclusion      Knockdown of SCIN inhibits the proliferation of GIST cells both in vitro and in vivo. Imatinib inhibits the expression of SCIN. SCIN may be a promising therapeutic target for GIST.