The expression and properties of alkaline phosphatase (ALP) in Eca109 cells, a cell line derived fromhuman esophageal cancer were studied with specific inhibition assay and polyacrylamide gel electrophoresis.The resul...The expression and properties of alkaline phosphatase (ALP) in Eca109 cells, a cell line derived fromhuman esophageal cancer were studied with specific inhibition assay and polyacrylamide gel electrophoresis.The results showed that ALP of Eca109 cells was heat stable and was strongly inhibited by L-pheuylalanine, but slightly inhibited by urea. Preduisolone could causedramatic increase in activity of ALP, but no change in ALP isozyme and concomitant increase in lactic dehydrogenase activity were found after prednisolone treatment. The results suggested that placental alkaline phosphatase as an oncodevelopmental gene product could be expressed ectopically by Eca109 cells and prednisolone could specifically induce increase in its activity.展开更多
BACKGROUND The poor prognosis and rising incidence of esophageal cancer highlight the need for improved therapeutics that are essential prior to treatment.LCL161 is an SMAC(second mitochondrial activator of caspases)m...BACKGROUND The poor prognosis and rising incidence of esophageal cancer highlight the need for improved therapeutics that are essential prior to treatment.LCL161 is an SMAC(second mitochondrial activator of caspases)mimic and inhibitor of apoptosis protein(IAP)antagonist which exhibits anti-tumor effects and improves the chemical sensitivity of many cancers.AIM To ascertain the effects and mechanisms of the SMAC analog LCL161 on esophageal cancer cells.METHODS MTT assay and TUNEL assay were used to detect cell proliferation and apoptosis,respectively.Western blot analysis was used to study the molecular mechanisms of LCL161-induced death of ECA109 cells.RESULTS LCL161 decreased ECA109 cell proliferation in dose-and time-dependent manner and induced apoptosis of ECA109 cells in a dose-dependent manner.Also,LCL161 induced a significant decrease in the expression of the XIAP and significant increase in the expression of Caspase-3.In addition,Bax increased significantly with increasing concentrations of LCL161,and the relative expression of Bax was significantly different between groups.CONCLUSION These findings support the hypothesis that LCL161 can inhibit proliferation and induce apoptosis in esophageal cancer cells by regulating the expression of IAP family members,suggesting that it has potential to be an effective treatment for esophageal squamous cell carcinoma.展开更多
目的探讨西红花苷对食管癌细胞细胞增殖、凋亡和侵袭的影响及其可能机制。方法以人食管癌Eca-109细胞为受试对象,采用CCK-8法检测不同浓度西红花苷对细胞的抑制作用,筛选最佳浓度和干预时间。将食管癌Eca-109细胞分为对照组、西红花低...目的探讨西红花苷对食管癌细胞细胞增殖、凋亡和侵袭的影响及其可能机制。方法以人食管癌Eca-109细胞为受试对象,采用CCK-8法检测不同浓度西红花苷对细胞的抑制作用,筛选最佳浓度和干预时间。将食管癌Eca-109细胞分为对照组、西红花低、中、高剂量组,分别按照0μmol/L、17μmol/L、34μmol/L、68μmol/L给予西红花苷干预,采用Transwell侵袭实验检测细胞侵袭能力;Western blot及RT-qPCR法分别检测各组细胞LKB1、AMPK、m TOR mRNA和蛋白表达水平。结果Transwell侵袭和细胞凋亡实验结果表明,与空白对照组比较,低、中、高剂量西红花苷组细胞穿过基膜的数量减少,凋亡率增高,差异有统计学意义(P<0.05或P<0.01);Western blot和RT-qPCR结果显示,与空白对照组比较,低、中、高剂量西红花苷组细胞LKB1、AMPK m RNA和蛋白表达水平升高,mTOR mRNA和蛋白表达水平降低,差异有统计学意义(P<0.05或P<0.01)。结论西红花苷对食管癌可能有抑制作用,其机制可能与调控LKB1/AMPK/mTOR信号通路相关。展开更多
文摘The expression and properties of alkaline phosphatase (ALP) in Eca109 cells, a cell line derived fromhuman esophageal cancer were studied with specific inhibition assay and polyacrylamide gel electrophoresis.The results showed that ALP of Eca109 cells was heat stable and was strongly inhibited by L-pheuylalanine, but slightly inhibited by urea. Preduisolone could causedramatic increase in activity of ALP, but no change in ALP isozyme and concomitant increase in lactic dehydrogenase activity were found after prednisolone treatment. The results suggested that placental alkaline phosphatase as an oncodevelopmental gene product could be expressed ectopically by Eca109 cells and prednisolone could specifically induce increase in its activity.
文摘BACKGROUND The poor prognosis and rising incidence of esophageal cancer highlight the need for improved therapeutics that are essential prior to treatment.LCL161 is an SMAC(second mitochondrial activator of caspases)mimic and inhibitor of apoptosis protein(IAP)antagonist which exhibits anti-tumor effects and improves the chemical sensitivity of many cancers.AIM To ascertain the effects and mechanisms of the SMAC analog LCL161 on esophageal cancer cells.METHODS MTT assay and TUNEL assay were used to detect cell proliferation and apoptosis,respectively.Western blot analysis was used to study the molecular mechanisms of LCL161-induced death of ECA109 cells.RESULTS LCL161 decreased ECA109 cell proliferation in dose-and time-dependent manner and induced apoptosis of ECA109 cells in a dose-dependent manner.Also,LCL161 induced a significant decrease in the expression of the XIAP and significant increase in the expression of Caspase-3.In addition,Bax increased significantly with increasing concentrations of LCL161,and the relative expression of Bax was significantly different between groups.CONCLUSION These findings support the hypothesis that LCL161 can inhibit proliferation and induce apoptosis in esophageal cancer cells by regulating the expression of IAP family members,suggesting that it has potential to be an effective treatment for esophageal squamous cell carcinoma.
文摘目的探讨西红花苷对食管癌细胞细胞增殖、凋亡和侵袭的影响及其可能机制。方法以人食管癌Eca-109细胞为受试对象,采用CCK-8法检测不同浓度西红花苷对细胞的抑制作用,筛选最佳浓度和干预时间。将食管癌Eca-109细胞分为对照组、西红花低、中、高剂量组,分别按照0μmol/L、17μmol/L、34μmol/L、68μmol/L给予西红花苷干预,采用Transwell侵袭实验检测细胞侵袭能力;Western blot及RT-qPCR法分别检测各组细胞LKB1、AMPK、m TOR mRNA和蛋白表达水平。结果Transwell侵袭和细胞凋亡实验结果表明,与空白对照组比较,低、中、高剂量西红花苷组细胞穿过基膜的数量减少,凋亡率增高,差异有统计学意义(P<0.05或P<0.01);Western blot和RT-qPCR结果显示,与空白对照组比较,低、中、高剂量西红花苷组细胞LKB1、AMPK m RNA和蛋白表达水平升高,mTOR mRNA和蛋白表达水平降低,差异有统计学意义(P<0.05或P<0.01)。结论西红花苷对食管癌可能有抑制作用,其机制可能与调控LKB1/AMPK/mTOR信号通路相关。
