【摘要】：目的:探討外源性信號(hào)素3A(Sema 3A)信號(hào)通路對(duì)轉(zhuǎn)化生長因子-β1(TGF-β1)誘導(dǎo)的肺癌A549細(xì)胞侵襲、增殖的影響及可能作用機(jī)制。方法:將肺癌A549細(xì)胞分為3組,即空白對(duì)照組、TGF-β1誘導(dǎo)組(TGF-β1組)、Sema 3A預(yù)處理組(Sema 3A+TGF-β1組)�？瞻讓�(duì)照組細(xì)胞正常培養(yǎng);TGF-β1組加入5μg·L~(-1)TGF-β1;Sema 3A+TGF-β1組首先加入10μmol·L~(-1)Sema 3A,預(yù)處理40~50 min后再加入5μg·L~(-1)TGF-β1。檢測細(xì)胞增殖、侵襲能力和E-cadherin、Akt、P-Akt蛋白表達(dá)。結(jié)果:Sema 3A+TGF-β1組細(xì)胞Sema 3A mRNA相對(duì)表達(dá)水平顯著高于空白對(duì)照組和TGF-β1組(均P0.05)。培養(yǎng)36 h~72 h內(nèi),TGF-β1組細(xì)胞增殖率顯著高于Sema 3A+TGF-β1組和空白對(duì)照組(均P0.05),Sema 3A+TGF-β1組細(xì)胞增殖率顯著高于空白對(duì)照組(均P0.05)。TGF-β1組穿透濾膜細(xì)胞數(shù)顯著高于Sema 3A+TGF-β1組和空白對(duì)照組(均P0.05),Sema 3A+TGF-β1組穿透濾膜細(xì)胞數(shù)顯著高于空白對(duì)照組(P0.05)。TGF-β1組E-cadherin蛋白表達(dá)顯著低于Sema 3A+TGF-β1組和空白對(duì)照組(均P0.05),P-Akt蛋白顯著高于Sema 3A+TGF-β1組和空白對(duì)照組(均P0.05);Sema 3A+TGF-β1組E-cadherin蛋白表達(dá)顯著低于空白對(duì)照組(P0.05),P-Akt顯著高于空白對(duì)照組(P0.05)。結(jié)論:Sema 3A能夠抑制TGF-β1誘導(dǎo)肺癌細(xì)胞侵襲、增殖的效應(yīng),其機(jī)制可能與抑制Akt磷酸化、上調(diào)E-cadherin表達(dá)有關(guān)。
[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.
【作者單位】： 湖北省腫瘤醫(yī)院胸部放療科;
【分類號(hào)】：R734.2

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