SOCS4在肺腺癌细胞增殖和侵袭中的作用

Effects of suppressor of cytokine signaling 4(SOCS4) on the proliferation and invasion of lung adenocarcinoma cells

目的探讨细胞因子信号抑制分子-4(SOCS4)对肺腺癌细胞生物学行为的影响及作用机制。方法采用基因干扰技术,用脂质体法转染SOCS4基因的干扰质粒到肺腺癌细胞系SPC-A1和A549中。CCK-8细胞增殖实验和Transwell实验分别检测SOCS4对肺腺癌细胞增殖和侵袭能力的影响,并通过western blot检测EGFR(表皮细胞因子受体)及其下游的磷酸化STAT3(p-STAT3,磷酸化的信号转导子与转录激活子)蛋白的表达水平。结果 CCK-8实验结果表明,SOCS4表达下调后,SPC-A1和A549细胞在第48、72、96和120 h的增殖能力均高于对照组(P均<0.05);Transwell实验结果显示,干扰组细胞侵袭的数量明显高于对照组(t=11.62,P<0.01;t=11.93,P<0.01)。western blot结果表明,干扰SOCS4表达能上调EGFR及其p-STAT3的表达。结论 SOCS4可能通过抑制EGFR表达并阻碍其下游的STAT3磷酸化,抑制肺腺癌细胞的增殖和侵袭。

Objective To investigate the effects of suppressor of cytokine signaling 4 （SOCS4） on the proliferation and invasion of lung adenocarcinoma cells, and its related mechanisms. Methods The interfering plasmids of SOCS4 gene were transiently transfected into lung adenocarcinoma SPC-A1 and A549 cells, respectively, by the lipofectamine 2000 reagent to reduce the expression of SOCS4. Then, the proliferation and invasion of SPC-A1 and A549 cells were detected by CCK-8 and Transwell assays, respectively, and the ex- pression levels of epidermal growth factor receptor （EGFR） and phosphorylated STAT3 （p-STAT3） by western blot. Results After down-regulating the expression level of SOCS4, the proliferation activities of SPC-A1 and A549 cells at 48, 72, 96 and 120 hours were significantly higher than those in the controls （ all P 〈 0.05 ） , and the invasion abilities of SPC-A1 and A549 cells were also significant- ly higher than those in the controls （t = 11.62 and 11.93, P 〈0.01 ）. Western blot results showed that the down-regulation of SOCS4 increased the expressions of EGFR and p-STAT3 obviously. Conclusion SOCS4 may inhibit the proliferation and invasion of lung ad- enocarcinoma cells by interfering the expression of EGFR and p-STAT3.