外源性信号素3A信号通路对转化生长因子-β1诱导肺癌细胞侵袭、增殖的影响
发布时间：2018-09-19 11:04
【摘要】：目的:探讨外源性信号素3A(Sema 3A)信号通路对转化生长因子-β1(TGF-β1)诱导的肺癌A549细胞侵袭、增殖的影响及可能作用机制。方法:将肺癌A549细胞分为3组,即空白对照组、TGF-β1诱导组(TGF-β1组)、Sema 3A预处理组(Sema 3A+TGF-β1组)。空白对照组细胞正常培养;TGF-β1组加入5μg·L~(-1)TGF-β1;Sema 3A+TGF-β1组首先加入10μmol·L~(-1)Sema 3A,预处理40~50 min后再加入5μg·L~(-1)TGF-β1。检测细胞增殖、侵袭能力和E-cadherin、Akt、P-Akt蛋白表达。结果:Sema 3A+TGF-β1组细胞Sema 3A mRNA相对表达水平显著高于空白对照组和TGF-β1组(均P0.05)。培养36 h~72 h内,TGF-β1组细胞增殖率显著高于Sema 3A+TGF-β1组和空白对照组(均P0.05),Sema 3A+TGF-β1组细胞增殖率显著高于空白对照组(均P0.05)。TGF-β1组穿透滤膜细胞数显著高于Sema 3A+TGF-β1组和空白对照组(均P0.05),Sema 3A+TGF-β1组穿透滤膜细胞数显著高于空白对照组(P0.05)。TGF-β1组E-cadherin蛋白表达显著低于Sema 3A+TGF-β1组和空白对照组(均P0.05),P-Akt蛋白显著高于Sema 3A+TGF-β1组和空白对照组(均P0.05);Sema 3A+TGF-β1组E-cadherin蛋白表达显著低于空白对照组(P0.05),P-Akt显著高于空白对照组(P0.05)。结论:Sema 3A能够抑制TGF-β1诱导肺癌细胞侵袭、增殖的效应,其机制可能与抑制Akt磷酸化、上调E-cadherin表达有关。
[Abstract]:Aim: to investigate the effect of exogenous signaling factor 3A (Sema 3A) on the invasion and proliferation of lung cancer A549 cells induced by transforming growth factor 尾 1 (TGF- 尾 1) and its possible mechanism. Methods: lung cancer A549 cells were divided into three groups: TGF- 尾 1 group (TGF- 尾 1 group) and Sema 3A TGF- 尾 1 group (Sema 3A TGF- 尾 1 group). TGF- 尾 1 group was treated with 5 渭 g L-1 TGF- 尾 1 TGF- 尾 1a TGF- 尾 1 group, 10 渭 mol L ~ (-1) Sema 3A was first added, 40 ~ (50) min was pretreated and 5 渭 g / L ~ (-1) TGF- 尾 _ (1) was added. Cell proliferation, invasion ability and the expression of E-cadherinus Akttfus P-Akt protein were detected. Results the relative expression level of Sema 3A mRNA was significantly higher in the group of Sema 3A TGF- 尾 1 than that in the control group and the group of TGF- 尾 1 (P0.05). The cell proliferation rate of TGF- 尾 1 group was significantly higher than that of Sema 3A TGF- 尾 1 group and blank control group (P0.05). The cell proliferation rate of Sema 3A TGF- 尾 1 group was significantly higher than that of blank control group (P0.05) .TGF- 尾 1 group was significantly higher than Sema 3A TGF- 尾 1 group and blank group. The expression of E-cadherin protein in Sema 3A TGF- 尾 1 group was significantly higher than that in the control group (P0.05). TGF- 尾 1 group was significantly lower than that in Sema 3A TGF- 尾 1 group and blank control group (P0.05) compared with Sema 3A TGF- 尾 1 group and blank control group (P0.05). The expression of P-Akt protein in Sema 3A TGF- 尾 1 group was significantly higher than that in Sema 3A TGF- 尾 1 group and blank control group (P0.05). The expression of E-cadherin protein was significantly lower than that of the blank control group (P0.05) and the expression of P-Akt was significantly higher than that of the blank control group (P0.05). ConclusionSema 3A can inhibit the invasion and proliferation of lung cancer cells induced by TGF- 尾 1, which may be related to the inhibition of Akt phosphorylation and the up-regulation of E-cadherin expression.
【作者单位】： 湖北省肿瘤医院胸部放疗科;
【分类号】：R734.2
[Abstract]:Aim: to investigate the effect of exogenous signaling factor 3A (Sema 3A) on the invasion and proliferation of lung cancer A549 cells induced by transforming growth factor 尾 1 (TGF- 尾 1) and its possible mechanism. Methods: lung cancer A549 cells were divided into three groups: TGF- 尾 1 group (TGF- 尾 1 group) and Sema 3A TGF- 尾 1 group (Sema 3A TGF- 尾 1 group). TGF- 尾 1 group was treated with 5 渭 g L-1 TGF- 尾 1 TGF- 尾 1a TGF- 尾 1 group, 10 渭 mol L ~ (-1) Sema 3A was first added, 40 ~ (50) min was pretreated and 5 渭 g / L ~ (-1) TGF- 尾 _ (1) was added. Cell proliferation, invasion ability and the expression of E-cadherinus Akttfus P-Akt protein were detected. Results the relative expression level of Sema 3A mRNA was significantly higher in the group of Sema 3A TGF- 尾 1 than that in the control group and the group of TGF- 尾 1 (P0.05). The cell proliferation rate of TGF- 尾 1 group was significantly higher than that of Sema 3A TGF- 尾 1 group and blank control group (P0.05). The cell proliferation rate of Sema 3A TGF- 尾 1 group was significantly higher than that of blank control group (P0.05) .TGF- 尾 1 group was significantly higher than Sema 3A TGF- 尾 1 group and blank group. The expression of E-cadherin protein in Sema 3A TGF- 尾 1 group was significantly higher than that in the control group (P0.05). TGF- 尾 1 group was significantly lower than that in Sema 3A TGF- 尾 1 group and blank control group (P0.05) compared with Sema 3A TGF- 尾 1 group and blank control group (P0.05). The expression of P-Akt protein in Sema 3A TGF- 尾 1 group was significantly higher than that in Sema 3A TGF- 尾 1 group and blank control group (P0.05). The expression of E-cadherin protein was significantly lower than that of the blank control group (P0.05) and the expression of P-Akt was significantly higher than that of the blank control group (P0.05). ConclusionSema 3A can inhibit the invasion and proliferation of lung cancer cells induced by TGF- 尾 1, which may be related to the inhibition of Akt phosphorylation and the up-regulation of E-cadherin expression.
【作者单位】： 湖北省肿瘤医院胸部放疗科;
【分类号】：R734.2
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