Objective To investigate the signaling pathway through testing the effects of dexamethasone (Dex) on the activation of the extracellular signal-regulated protein kinase 1/2 (ERK1/2) and p38 kinase (p38) in HO-8910...Objective To investigate the signaling pathway through testing the effects of dexamethasone (Dex) on the activation of the extracellular signal-regulated protein kinase 1/2 (ERK1/2) and p38 kinase (p38) in HO-8910 cells.Methods Activation of the ERK1/2 and p38 was detected by Western blotting using the antibodies against the total ERK1/2 and p38 mitogen-activated protein kinases (MAPKs) protein and the phosphorylated forms of them. Results Dex could suppress the activation of ERK1/2, while enhance the activation of p38 rapidly and strongly in a dose- and time- dependent manner. Neither effect could be blocked by RU486, the antagonist of glucocorticoid receptor (GR).Conclusion Dex has rapid effects on the activation of ERK1/2 and p38, and these effects are not mediated by GR.展开更多
目的探讨上皮性细胞粘附分子(E-cadherin,E-cad)在人卵巢浆液性囊腺癌高低转移细胞株HO-8910PM及HO-8910中的表达及生物学行为的差异。方法采用免疫荧光法及W estern b lotting检测细胞中E-cad蛋白表达的差异,用粘附实验检测细胞与细胞...目的探讨上皮性细胞粘附分子(E-cadherin,E-cad)在人卵巢浆液性囊腺癌高低转移细胞株HO-8910PM及HO-8910中的表达及生物学行为的差异。方法采用免疫荧光法及W estern b lotting检测细胞中E-cad蛋白表达的差异,用粘附实验检测细胞与细胞外基质的粘附能力,用Transwell小室法检测细胞侵袭能力及迁移能力。结果E-cad在HO-8910细胞中为高表达,在HO-8910PM细胞中为低表达,HO-8910PM细胞与细胞外基质的粘附能力、侵袭能力及迁移能力均明显高于HO-8910细胞(P<0.05,P<0.01)。结论人卵巢浆液性曩腺癌HO-8910PM细胞的浸润、转移等恶性行为可能与E-cad的表达下降有关。展开更多
文摘Objective To investigate the signaling pathway through testing the effects of dexamethasone (Dex) on the activation of the extracellular signal-regulated protein kinase 1/2 (ERK1/2) and p38 kinase (p38) in HO-8910 cells.Methods Activation of the ERK1/2 and p38 was detected by Western blotting using the antibodies against the total ERK1/2 and p38 mitogen-activated protein kinases (MAPKs) protein and the phosphorylated forms of them. Results Dex could suppress the activation of ERK1/2, while enhance the activation of p38 rapidly and strongly in a dose- and time- dependent manner. Neither effect could be blocked by RU486, the antagonist of glucocorticoid receptor (GR).Conclusion Dex has rapid effects on the activation of ERK1/2 and p38, and these effects are not mediated by GR.
文摘目的探讨上皮性细胞粘附分子(E-cadherin,E-cad)在人卵巢浆液性囊腺癌高低转移细胞株HO-8910PM及HO-8910中的表达及生物学行为的差异。方法采用免疫荧光法及W estern b lotting检测细胞中E-cad蛋白表达的差异,用粘附实验检测细胞与细胞外基质的粘附能力,用Transwell小室法检测细胞侵袭能力及迁移能力。结果E-cad在HO-8910细胞中为高表达,在HO-8910PM细胞中为低表达,HO-8910PM细胞与细胞外基质的粘附能力、侵袭能力及迁移能力均明显高于HO-8910细胞(P<0.05,P<0.01)。结论人卵巢浆液性曩腺癌HO-8910PM细胞的浸润、转移等恶性行为可能与E-cad的表达下降有关。
