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.