BACKGROUND Cell division cyclin 25C(CDC25C)is a protein that plays a critical role in the cell cycle,specifically in the transition from the G2 phase to the M phase.Recent research has shown that CDC25C could be a pot...BACKGROUND Cell division cyclin 25C(CDC25C)is a protein that plays a critical role in the cell cycle,specifically in the transition from the G2 phase to the M phase.Recent research has shown that CDC25C could be a potential therapeutic target for cancers,particularly for hepatocellular carcinoma(HCC).However,the specific regulatory mechanisms underlying the role of CDC25C in HCC tumorigenesis and development remain incompletely understood.AIM To explore the impact of CDC25C on cell proliferation and apoptosis,as well as its regulatory mechanisms in HCC development.METHODS Hepa1-6 and B16 cells were transduced with a lentiviral vector containing shRNA interference sequences(LV-CDC25C shRNA)to knock down CDC25C.Subsequently,a xenograft mouse model was established by subcutaneously injecting transduced Hepa1-6 cells into C57BL/6 mice to assess the effects of CDC25C knockdown on HCC development in vivo.Cell proliferation and migration were evaluated using a Cell Counting Kit-8 cell proliferation assays and wound healing assays,respectively.The expression of endoplasmic reticulum(ER)stress-related molecules(glucose-regulated protein 78,X-box binding protein-1,and C/EBP homologous protein)was measured in both cells and subcutaneous xenografts using quantitative real-time PCR(qRT-PCR)and western blotting.Additionally,apoptosis was investigated using flow cytometry,qRT-PCR,and western blotting.RESULTS CDC25C was stably suppressed in Hepa1-6 and B16 cells through LV-CDC25C shRNA transduction.A xenograft model with CDC25C knockdown was successfully established and that downregulation of CDC25C expression significantly inhibited HCC growth in mice.CDC25C knockdown not only inhibited cell proliferation and migration but also significantly increased the ER stress response,ultimately promoting ER stress-induced apoptosis in HCC cells.CONCLUSION The regulatory mechanism of CDC25C in HCC development may involve the activation of ER stress and the ER stress-induced apoptosis signaling pathway.展开更多
目的探索胃癌、慢性胃病患者脾证分型与 cyclin E 表达的关系.方法在胃癌和慢性胃病患者中,选取具有中医脾虚表现的脾气(阳)虚、脾阴虚患者,和具有脾实表现的脾胃湿热、寒湿困脾证患者,以及按慢性浅表性胃炎、肠上皮化生、不典型增生、...目的探索胃癌、慢性胃病患者脾证分型与 cyclin E 表达的关系.方法在胃癌和慢性胃病患者中,选取具有中医脾虚表现的脾气(阳)虚、脾阴虚患者,和具有脾实表现的脾胃湿热、寒湿困脾证患者,以及按慢性浅表性胃炎、肠上皮化生、不典型增生、胃癌分组的患者,进行胃粘膜组织 cyclin E 免疫组化染色;对各证型的 cyclin E 表达进行比较,并分析 cyclin E 在常见胄粘膜病变中表达的差异.结果 cyclin E 在上述四种脾证分型的表达有显著性差异,阳性百分率分别为7.9%,27.3%,31.4%和14.3%.在慢性浅表性胄炎、肠上皮化生、不典型增生和胃癌的表达也有显著性差异,阳性率分别为7.5%,28.6%,37.9%和42.6%,后两者已较接近.结论胃癌和慢性胃病患者中,不同的中医脾证其 cyclin E 表达明显不同,在脾胃湿热和睥阴虚证型中较高,在寒湿困脾和脾气(阳)虚证型中较低.cyclin E 表达随病变由慢性浅表性胃炎、癌前病变到癌而逐渐增高,其与胃癌的发生发展密切相关.展开更多
基金Supported by Natural Science Foundation of Guangxi Zhuang Autonomous Region,China,No.2023GXNSFAA026070 and No.2018GXNSFAA281071.
文摘BACKGROUND Cell division cyclin 25C(CDC25C)is a protein that plays a critical role in the cell cycle,specifically in the transition from the G2 phase to the M phase.Recent research has shown that CDC25C could be a potential therapeutic target for cancers,particularly for hepatocellular carcinoma(HCC).However,the specific regulatory mechanisms underlying the role of CDC25C in HCC tumorigenesis and development remain incompletely understood.AIM To explore the impact of CDC25C on cell proliferation and apoptosis,as well as its regulatory mechanisms in HCC development.METHODS Hepa1-6 and B16 cells were transduced with a lentiviral vector containing shRNA interference sequences(LV-CDC25C shRNA)to knock down CDC25C.Subsequently,a xenograft mouse model was established by subcutaneously injecting transduced Hepa1-6 cells into C57BL/6 mice to assess the effects of CDC25C knockdown on HCC development in vivo.Cell proliferation and migration were evaluated using a Cell Counting Kit-8 cell proliferation assays and wound healing assays,respectively.The expression of endoplasmic reticulum(ER)stress-related molecules(glucose-regulated protein 78,X-box binding protein-1,and C/EBP homologous protein)was measured in both cells and subcutaneous xenografts using quantitative real-time PCR(qRT-PCR)and western blotting.Additionally,apoptosis was investigated using flow cytometry,qRT-PCR,and western blotting.RESULTS CDC25C was stably suppressed in Hepa1-6 and B16 cells through LV-CDC25C shRNA transduction.A xenograft model with CDC25C knockdown was successfully established and that downregulation of CDC25C expression significantly inhibited HCC growth in mice.CDC25C knockdown not only inhibited cell proliferation and migration but also significantly increased the ER stress response,ultimately promoting ER stress-induced apoptosis in HCC cells.CONCLUSION The regulatory mechanism of CDC25C in HCC development may involve the activation of ER stress and the ER stress-induced apoptosis signaling pathway.
文摘目的探索胃癌、慢性胃病患者脾证分型与 cyclin E 表达的关系.方法在胃癌和慢性胃病患者中,选取具有中医脾虚表现的脾气(阳)虚、脾阴虚患者,和具有脾实表现的脾胃湿热、寒湿困脾证患者,以及按慢性浅表性胃炎、肠上皮化生、不典型增生、胃癌分组的患者,进行胃粘膜组织 cyclin E 免疫组化染色;对各证型的 cyclin E 表达进行比较,并分析 cyclin E 在常见胄粘膜病变中表达的差异.结果 cyclin E 在上述四种脾证分型的表达有显著性差异,阳性百分率分别为7.9%,27.3%,31.4%和14.3%.在慢性浅表性胄炎、肠上皮化生、不典型增生和胃癌的表达也有显著性差异,阳性率分别为7.5%,28.6%,37.9%和42.6%,后两者已较接近.结论胃癌和慢性胃病患者中,不同的中医脾证其 cyclin E 表达明显不同,在脾胃湿热和睥阴虚证型中较高,在寒湿困脾和脾气(阳)虚证型中较低.cyclin E 表达随病变由慢性浅表性胃炎、癌前病变到癌而逐渐增高,其与胃癌的发生发展密切相关.
