[目的]研究ASPM对非小细胞肺癌A549细胞发展的影响。[方法]通过免疫组化实验分析ASPM在非小细胞肺癌组织中的表达;将非小细胞肺癌A549细胞随机分为3个实验组:si NC实验组、si ASPM实验组与BPD-MA实验组。通过CCK-8实验检测A549细胞的增...[目的]研究ASPM对非小细胞肺癌A549细胞发展的影响。[方法]通过免疫组化实验分析ASPM在非小细胞肺癌组织中的表达;将非小细胞肺癌A549细胞随机分为3个实验组:si NC实验组、si ASPM实验组与BPD-MA实验组。通过CCK-8实验检测A549细胞的增殖速度;通过Transwell实验检测A549细胞的侵袭能力;通过流式细胞术检测A549细胞的凋亡率;采用蛋白免疫印迹方法分析A549细胞中YAP1/TAZ通路蛋白的表达。[结果]与癌旁组织比较,ASPM在非小细胞肺癌组织中表达增加(0.28±0.09 vs 0.81±0.06,P<0.05)。与si NC实验组比较,si ASPM以及BPD-MA实验组的A549细胞增殖能力减弱(2.23±0.07 vs 1.16±0.03 vs 1.13±0.05,P<0.05);si ASPM以及BPD-MA实验组的A549细胞侵袭数量减少(126.08±9.33 vs 68.51±7.21 vs 72.82±10.55,P<0.05);si ASPM以及BPD-MA实验组的A549细胞凋亡率增加[(3.22±0.73)%vs(17.01±5.26)%vs(19.23±8.68)%,P<0.05];si ASPM以及BPD-MA实验组的A549细胞YAP1、TAZ蛋白表达下调(0.87±0.03 vs 0.35±0.07 vs 0.33±0.06;0.91±0.12 vs 0.26±0.09 vs 0.31±0.03,P<0.05)。[结论]抑制ASPM表达后,A549细胞的增殖能力与侵袭数量降低,凋亡率增加,该过程与ASPM调节YAP1/TAZ信号通路相关。展开更多
The development of a cerebral organoid culture in vitro offers an opportunity to generate human brain-like organs to investigate mechanisms of human disease that are specific to the neurogenesis of radial glial （RG）...The development of a cerebral organoid culture in vitro offers an opportunity to generate human brain-like organs to investigate mechanisms of human disease that are specific to the neurogenesis of radial glial （RG） and outer radial glial （oRG） cells in the ventrJcular zone （VZ） and subventricular zone （SVZ） of the developing neocortex. Modeling neuronal progenitors and the organization that produces mature subcortical neuron subtypes during early stages of development is essential for studying human brain developmental diseases. Several previous efforts have shown to grow neural organoid in culture dishes successfully, however we demonstrate a new paradigm that recapitulates neocortical development process with VZ, OSVZ formation and the lamination organization of cortical layer structure. In addition, using patient.specific induced pluripotent stem cells （iPSCs） with dysfunction of the Aspm gene from a primary microcephaly patient, we demonstrate neurogenesis defects result in defective neuronal activity in patient organoids, suggesting a new strategy to study human developmental diseases in central nerve system.展开更多
文摘[目的]研究ASPM对非小细胞肺癌A549细胞发展的影响。[方法]通过免疫组化实验分析ASPM在非小细胞肺癌组织中的表达;将非小细胞肺癌A549细胞随机分为3个实验组:si NC实验组、si ASPM实验组与BPD-MA实验组。通过CCK-8实验检测A549细胞的增殖速度;通过Transwell实验检测A549细胞的侵袭能力;通过流式细胞术检测A549细胞的凋亡率;采用蛋白免疫印迹方法分析A549细胞中YAP1/TAZ通路蛋白的表达。[结果]与癌旁组织比较,ASPM在非小细胞肺癌组织中表达增加(0.28±0.09 vs 0.81±0.06,P<0.05)。与si NC实验组比较,si ASPM以及BPD-MA实验组的A549细胞增殖能力减弱(2.23±0.07 vs 1.16±0.03 vs 1.13±0.05,P<0.05);si ASPM以及BPD-MA实验组的A549细胞侵袭数量减少(126.08±9.33 vs 68.51±7.21 vs 72.82±10.55,P<0.05);si ASPM以及BPD-MA实验组的A549细胞凋亡率增加[(3.22±0.73)%vs(17.01±5.26)%vs(19.23±8.68)%,P<0.05];si ASPM以及BPD-MA实验组的A549细胞YAP1、TAZ蛋白表达下调(0.87±0.03 vs 0.35±0.07 vs 0.33±0.06;0.91±0.12 vs 0.26±0.09 vs 0.31±0.03,P<0.05)。[结论]抑制ASPM表达后,A549细胞的增殖能力与侵袭数量降低,凋亡率增加,该过程与ASPM调节YAP1/TAZ信号通路相关。
文摘The development of a cerebral organoid culture in vitro offers an opportunity to generate human brain-like organs to investigate mechanisms of human disease that are specific to the neurogenesis of radial glial （RG） and outer radial glial （oRG） cells in the ventrJcular zone （VZ） and subventricular zone （SVZ） of the developing neocortex. Modeling neuronal progenitors and the organization that produces mature subcortical neuron subtypes during early stages of development is essential for studying human brain developmental diseases. Several previous efforts have shown to grow neural organoid in culture dishes successfully, however we demonstrate a new paradigm that recapitulates neocortical development process with VZ, OSVZ formation and the lamination organization of cortical layer structure. In addition, using patient.specific induced pluripotent stem cells （iPSCs） with dysfunction of the Aspm gene from a primary microcephaly patient, we demonstrate neurogenesis defects result in defective neuronal activity in patient organoids, suggesting a new strategy to study human developmental diseases in central nerve system.
