Abstract:Objective: To investigate the effect of suppressor of cytokine signaling 2 (SOCS2) overexpression on the growth, movement and JAK2/STAT3 pathway of rectal cancer cells. Methods: HCT8 cells were divided into control group, pcDNA group and pcDNA-SOCS2 group, transfected with pcDNA empty vector or pcDNA-SOCS2 group recombinant expression vector according to different groups. SOCS2 gene expression was detected by RT-PCR, cell proliferation was detected by BrdU staining, flow cytometry was used to detect apoptosis, Transwell method was used to detect cell invasion, and Western blot was used to detect SOCS2, E-cadherin, vimentin, fibronectin protein expression, and phosphorylation of JAK2 and STAT3. In addition, BALB/c nu/nu nude mice were divided into con-trol group and pcDNA-SOCS2 group. HCT8 subcutaneous xenograft model was established, and the weight of xenograft tumor was weighed. The average optical density of Ki-67 and vascular endothelial growth factor (VEGF) was measured by immunohistochemistry, and the Western blot was used to detect the phosphorylation of JAK2 and STAT3 in tumor tissues. Results: In the ex-vivo experiment, the RT-PCR results showed that compared with the control group (1.00±0.00), the SOCS2 mRNA level (4.70±0.27) of the pcDNA-SOCS2 group was significantly increased (P=0.000). Western blot results showed that the expression of SOCS2 protein in the pcDNA-SOCS2 group (0.130±0.020) was significantly up-regulated (P=0.000) compared with that in the control group (0.010±0.005). The percentage of BrdU positive was signifi-cantly reduced (P=0.000); flow cytometry results showed that the apoptosis rate of HCT8 cells in the pcDNA-SOCS2 group [(35.0±5.0) %] was significantly higher than that in the control group [(6.0±3.4) %, P=0.000]. Transwell analysis results showed that the number of HCT8 cell invasions in the pcDNA-SOCS2 group (89.0±10.0) was significantly lower than that of the control group (87.0±13.0, P=0.000). Western blot results showed that the E-cadherin protein level (0.120±0.030) of HCT8 cells in the pcDNA-SOCS2 group was significantly increased compared to the con-trol group (0.010±0.004, P=0.000), while the Vimentin protein level (0.008±0.004) and Fibronectin protein level (0.010±0.005) were significantly reduced compared to the control group (0.170±0.024, 0.070±0.020), P=0.000, the phosphorylation level of JAK2 and STAT3 decreased (P=0.000). In the in-vivo experiment, the tumor weight in the pcDNA-SOCS2 group (0.14±0.06) was signifi-cantly less than that in the control group (0.45±0.08, P=0.000). The results of immunohistochemistry showed that the average optical density of Ki-67 and VEGF in the pcDNA-SOCS2 group (17.0±6.0, 7.0±6.0) was significantly lower than that in the control group (52.0±9.0, 43.0±9.0, P=0.000), and the phosphorylation levels of JAK2 and STAT3 tumor bodies were significantly down-regulated (P=0.000). Conclusion: The overexpression of SOCS2 can inhibit the proliferation and exercise ability of rectal cancer HCT8 cells and promote the apoptosis, which is related to JAK2/STAT3 pathway.
