[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
Dengue virus(DENV)remains a pervasive global health threat,further complicated by the occurrence of neutropenia-a distinct clinical feature indicative of an altered host immune response,closely correlated with progres...Dengue virus(DENV)remains a pervasive global health threat,further complicated by the occurrence of neutropenia-a distinct clinical feature indicative of an altered host immune response,closely correlated with progressive disease deterioration and increased severity.Nevertheless,the molecular mechanisms underlying dengue-associated neutropenia remain inadequately elucidated.In this study,the comprehensive plasma proteomic profiling of dengue fever(DF)patients,DF patients with neutropenia(DFN),and healthy controls(HC)was systematically analyzed using a deep dataindependent acquisition(DIA)workflow combined with LC-MS/MS analysis,to elucidate key cellular pathways and identify promising biomarkers.DFN patients exhibited significant dual hematological alterations,with notable changes in both platelet and neutrophil counts,reflecting a complex disturbance in hematological homeostasis during dengue progression.DIA analysis quantified 2475 proteins,revealing widespread proteomic alterations among the DF,DFN,and HC subjects.Differential analysis highlighted significant fluctuations in proteins related to cytoskeletal organization,metabolic regulation,and intracellular signaling.Enrichment analyses implicated pathways such as focal adhesion,platelet activation,and PI3K-Akt signaling.Machine learning methods further identified a panel of four biomarkers-CNST,DSTN,DUSP3,and PDIA5-with high predictive accuracy for dengue diagnosis and subgroup differentiation.In conclusion,this study advances our understanding of dengue’s plasma proteomic landscape and underscores the synergistic potential of DIA-based proteomics and machine learning in unveiling host-response mechanisms,thereby informing early diagnosis and targeted therapeutic strategies.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。
基金supported by National Key R&D Program of China(2023YFA0915600)Guangdong Basic and Applied Basic Research Foundation(2025B1515020010)+3 种基金Shenzhen Clinical Research Center for Emerging Infectious Diseases(LCYSSQ20220823091203007)Sanming Project of Medicine in Shenzhen(SZSM202311033)Shenzhen Fund for Guangdong Provincial High-level Clinical Key Specialties(No.SZGSP011)Shenzhen High-level Hospital Construction Fund(XKJSCRGRK-006).
文摘Dengue virus(DENV)remains a pervasive global health threat,further complicated by the occurrence of neutropenia-a distinct clinical feature indicative of an altered host immune response,closely correlated with progressive disease deterioration and increased severity.Nevertheless,the molecular mechanisms underlying dengue-associated neutropenia remain inadequately elucidated.In this study,the comprehensive plasma proteomic profiling of dengue fever(DF)patients,DF patients with neutropenia(DFN),and healthy controls(HC)was systematically analyzed using a deep dataindependent acquisition(DIA)workflow combined with LC-MS/MS analysis,to elucidate key cellular pathways and identify promising biomarkers.DFN patients exhibited significant dual hematological alterations,with notable changes in both platelet and neutrophil counts,reflecting a complex disturbance in hematological homeostasis during dengue progression.DIA analysis quantified 2475 proteins,revealing widespread proteomic alterations among the DF,DFN,and HC subjects.Differential analysis highlighted significant fluctuations in proteins related to cytoskeletal organization,metabolic regulation,and intracellular signaling.Enrichment analyses implicated pathways such as focal adhesion,platelet activation,and PI3K-Akt signaling.Machine learning methods further identified a panel of four biomarkers-CNST,DSTN,DUSP3,and PDIA5-with high predictive accuracy for dengue diagnosis and subgroup differentiation.In conclusion,this study advances our understanding of dengue’s plasma proteomic landscape and underscores the synergistic potential of DIA-based proteomics and machine learning in unveiling host-response mechanisms,thereby informing early diagnosis and targeted therapeutic strategies.
