Figure 6.

Manipulation of SOCS2 expression alters the proliferation of AGS cells. Knockdown of SOCS2 in AGS-WT cells promoted cell proliferation in AGS cells. Cells were treated with SOCS2-siRNA to knock down SOCS2. Cells treated with a non-specific control siRNA were used as controls. AGS cell treatment with SOCS2-siRNA significantly knocked down SOCS2 expression in AGS-WT cells at (A) RNA and (B) protein levels. *P<0.05 vs. Ctrl siRNA. (C) A significantly higher cell proliferation rate was detected by using an MTS assay in cells treated with siRNA-SOCS2 when compared with cells treated with Ctrl-siRNA. *P<0.05 vs. Ctrl siRNA. Overexpression of SOCS2 inhibited cell AGS cell proliferation. Cells were transfected with pCMV6-SOCS2 (full-length-SOCS2) to overexpress SOCS2. Cells treated with the pCMV6 empty vector were used as controls. SOCS2 overexpression in AGS-WT cells following transfection of pCMV6-SOCS2 was confirmed via reverse transcription-quantitative PCR and western blotting, respectively, at (D) RNA and (E) protein levels. *P<0.05 vs. pCMV6-Ctrl. A significantly lower cell proliferation rate was detected using an MTS assay in cells transfected with pCMV6-SOCS2 compared with pCMV6 empty vector-treated cells (F) Representative blotting images are presented in B and E. Densitometric levels of positive band for SOCS2 were quantified and are expressed as the ratio to GAPDH. *P<0.05 vs. pCMV6-Ctrl. SOCS, suppressor of cytokine signaling; WT, wild type; siRNA, small interfering RNA; Ctrl, control; OD, optical density.