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作 者:李蒙 贺德[1] 马广念[1] 李志坚 邓思远 Li Meng;He De;Ma Guangnian;Li Zhijian;Deng Siyuan(Department of General Surgery, Affiliated Baoan Hospital of Southern Medical University, Shenzhen 518101, China;Graduate School, Guangdong Medical University, Zhanjiang 524023, China)
机构地区:[1]南方医科大学附属深圳宝安医院普通外科,深圳518101 [2]广东医科大学研究生院,湛江524023
出 处:《中华实验外科杂志》2019年第4期612-614,共3页Chinese Journal of Experimental Surgery
基 金:深圳市科技创新委员会基础研究项目(JCYJ20160427192617570).
摘 要:目的观察盐诱导激酶1(SIK1)对胰腺癌细胞增殖、迁移和侵袭的调控作用。方法将SIK1模拟物转染胰腺癌细胞株HPAC、BxPC3和PANC-1,48 h后,实时定量聚合酶链反应(Real-time PCR)检测SIK1的表达,细胞计数试剂盒(CCK-8)检测SIK1对细胞增殖的作用,细胞划痕实验检测细胞的迁移能力,Transwell实验检测细胞的侵袭能力。结果SIK1在胰腺癌HPAC、BxPC3和PANC-1细胞中相对表达低于正常胰腺细胞(0.16±0.06、0.16±0.03和0.19±0.03,P<0.01);转染SIK1模拟物后,胰腺癌HPAC、BxPC3和PANC-1细胞内SIK1相对表达量明显升高(3.66±0.49、1.91±0.35和2.04±0.19,P<0.01)。过表达SIK1后,CCK-8实验结果显示,明显降低HPAC、BxPC3和PANC-1细胞的增殖(0.67±0.02比0.61±0.03,P<0.01;0.79±0.03比0.70±0.02,P<0.01;0.87±0.02比0.75±0.03,P<0.01);划痕实验结果显示:明显抑制HPAC、BxPC3和PANC-1细胞迁移[(169.82±7.76)比(106.89±7.79)μm,P<0.01;(106.95±6.29)比(62.79±9.55)μm,P<0.01;(105.38±7.54)比(82.41±10.74)μm,P<0.01];Transwell细胞侵袭实验显示:明显抑制HPAC、BxPC3和PANC-1细胞侵袭[(63.50±3.51)比(47.83±3.19)个,P<0.01;(34.50±3.94)比(21.50±2.51)个,P<0.01;(52.50±2.43)比(32.83±2.14)个,P<0.01]。结论过表达SIK1后抑制HPAC、BxPC3和PANC-1细胞株增殖、迁移和侵袭的作用。Objective To investigate the effect of salt-induced kinase 1 (SIK1) on the proliferation, migration and invasion of pancreatic cells. Methods SIK1-mimic was transfected into HPAC, BxPC3 and PANC-1 cell lines. The expression of SIK1 was detected by real-time quantitative polymerase chain reaction (Real-time PCR) after 48 h. Cell proliferation was measured by cell counting kit-8 (CCK-8). The migration ability was assayed by would healing test. Transwell invasion assay was used to measure cell invasion Results The expression of SIK1 in HPAC, BxPC3 and PANC-1 cells was significantly lower than that in normal pancreatic cells (0.16±0.06, 0.16±0.03, 0.19±0.03, P<0.01). The expression of SIK1 in HPAC, BxPC3 and PANC-1 cells was significantly higher (3.66±0.49, 1.91±0.35 and 2.04±0.19, P<0.01) after transfection with SIK1 mimic. CCK-8 results showed that the proliferation of HPAC, BxPC3 and PANC-1 cells was significantly reduced (0.67±0.02 vs. 0.61±0.03, P<0.01;0.79±0.03 vs. 0.70±0.02, P<0.01;0.87±0.02 vs. 0.75±0.03, P<0.01). The results of wound healing test showed that the migration of HPAC, BxPC3 and PANC-1 cells was inhibited [(169.82±7.76) vs.(106.89±7.79)μm, P<0.01;(106.95±6.29) vs.(62.79±9.55)μm, P<0.01;(105.38±7.54) vs.(82.41±10.74)μm, tPACN-1=4.287, P<0.01]. Transwell cell invasion assay showed significant inhibition of HPAC, BxPC3 and PANC-1 cell invasion [(63.50±3.51) vs.(47.83±3.19), P<0.01;(34.50±3.94) vs.(21.50±2.51), P<0.01;(52.50±2.43) vs.(32.83±2.14), P<0.01]. Conclusion Overexpression of SIK1 inhibited the proliferation, migration and invasion of HPAC, BxPC3 and PANC-1 cell lines.
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