BACKGROUND Centromere protein A(CENPA)exhibits an increased expression level in primary human rectal cancer tissues,but its role has not been investigated.AIM To clarify the specific role and mechanism of CENPA in rec...BACKGROUND Centromere protein A(CENPA)exhibits an increased expression level in primary human rectal cancer tissues,but its role has not been investigated.AIM To clarify the specific role and mechanism of CENPA in rectal cancer progression.METHODS CENPA protein expression in rectal cancer tissues and cell lines were detected.CENPA was overexpressed and knocked down in SW837 and SW480 cells,and proliferation,invasion,apoptosis and epithelial-mesenchymal transition(EMT)marker protein levels were examined.O6-methylguanine DNA methyltransferase(MGMT)promoter methylation was assessed with methylation-specific poly-merase chain reaction.Co-immunoprecipitation assay verified the interaction between MGMT and protein tyrosine phosphatase nonreceptor type 4(PTPN4).SW837 cells with CENPA knockdown were injected subcutaneously into mice,and tumor growth was examined.RESULTS CENPA was upregulated in rectal cancer tissues and cell lines.CENPA overex-pression promoted proliferation,invasion and EMT,and inhibited apoptosis in rectal cancer cells.Whereas CENPA knockdown showed the opposite results.Moreover,CENPA inhibited MGMT expression by promoting DNA methyltrans-ferase 1-mediated MGMT promoter methylation.MGMT knockdown abolished the CENPA knockdown-mediated inhibition of rectal cancer cell progression.MGMT increased PTPN4 protein stability by inhibiting PTPN4 ubiquitination degradation via competing with ubiquitin-conjugating enzyme E2O for interacting with PTPN4.PTPN4 knockdown abolished the inhibitory effects of MGMT overexpression on rectal cancer cell progression.Moreover,CENPA knockdown inhibited xenograft tumor growth in vivo.CONCLUSION CENPA knockdown inhibited rectal cancer cell growth and attenuated xenograft tumor growth through regulating the MGMT/PTPN4 axis.展开更多
通过水热法制备Bi2WO6、热分解法制备α-Fe2O3,并利用机械混合的方式获得α-Fe2O3/Bi2WO6复合材料。利用XRD、UV-Vis、BET、SEM、XPS对样品进行表征,相比Bi2WO6,α-Fe2O3/Bi2WO6复合结构在可见光区域的吸收带变宽。在α-Fe2O3/Bi2WO6+H...通过水热法制备Bi2WO6、热分解法制备α-Fe2O3,并利用机械混合的方式获得α-Fe2O3/Bi2WO6复合材料。利用XRD、UV-Vis、BET、SEM、XPS对样品进行表征,相比Bi2WO6,α-Fe2O3/Bi2WO6复合结构在可见光区域的吸收带变宽。在α-Fe2O3/Bi2WO6+H2O2光催化系统中,紫外光照射30 min MO完全降解;模拟太阳光照射60 min MO降解率达到85%,高于单独的Bi2WO6和α-Fe2O3。优良的光催化活性是由于光生电子从α-Fe2O3的导带迁移到Bi2WO6的导带,有效避免了光生电子-空穴的复合,从而提升了光催化效率;在α-Fe2O3/Bi2WO6+H2O2系统中,H2O2作为电子受体,H2O作为空穴受体,能够产生更多的羟基自由基,促进MO降解。展开更多
基金This study was reviewed and approved by the Ethic Committee of Medical College of Henan Vocational University of Science and Technology(Approval No.HVUYL414101416920231017001)all participants signed a written informed consent.
文摘BACKGROUND Centromere protein A(CENPA)exhibits an increased expression level in primary human rectal cancer tissues,but its role has not been investigated.AIM To clarify the specific role and mechanism of CENPA in rectal cancer progression.METHODS CENPA protein expression in rectal cancer tissues and cell lines were detected.CENPA was overexpressed and knocked down in SW837 and SW480 cells,and proliferation,invasion,apoptosis and epithelial-mesenchymal transition(EMT)marker protein levels were examined.O6-methylguanine DNA methyltransferase(MGMT)promoter methylation was assessed with methylation-specific poly-merase chain reaction.Co-immunoprecipitation assay verified the interaction between MGMT and protein tyrosine phosphatase nonreceptor type 4(PTPN4).SW837 cells with CENPA knockdown were injected subcutaneously into mice,and tumor growth was examined.RESULTS CENPA was upregulated in rectal cancer tissues and cell lines.CENPA overex-pression promoted proliferation,invasion and EMT,and inhibited apoptosis in rectal cancer cells.Whereas CENPA knockdown showed the opposite results.Moreover,CENPA inhibited MGMT expression by promoting DNA methyltrans-ferase 1-mediated MGMT promoter methylation.MGMT knockdown abolished the CENPA knockdown-mediated inhibition of rectal cancer cell progression.MGMT increased PTPN4 protein stability by inhibiting PTPN4 ubiquitination degradation via competing with ubiquitin-conjugating enzyme E2O for interacting with PTPN4.PTPN4 knockdown abolished the inhibitory effects of MGMT overexpression on rectal cancer cell progression.Moreover,CENPA knockdown inhibited xenograft tumor growth in vivo.CONCLUSION CENPA knockdown inhibited rectal cancer cell growth and attenuated xenograft tumor growth through regulating the MGMT/PTPN4 axis.
文摘为研究稀土发光纳米晶的微观结构和形貌对发光性能的影响,用凝胶-微波干燥法和凝胶-烘箱干燥法制备了花状形貌的Sr3Al2O6晶体.研究了微波干燥和烘箱干燥两种不同的干燥方式对溶胶-凝胶法制备的Sr3Al2O6∶Eu2+发光粉体粒径、形貌、团聚程度、干燥时间及发光性能等的影响,结果表明采用微波干燥不仅可以大大缩短干燥所需时间,而且有利于减弱Sr3Al2O6∶Eu2+发光粉料的团聚和团聚程度,制得了颗粒分散均匀、团聚程度低、发光强度高的Sr3Al2O6∶Eu2+花状形貌粉体.研究了Sr3Al2O6∶Eu2+发光粉体的新型形貌对发光性能的影响,微波干燥法制备的均匀分散的花状形貌发光粉体发光强度高,余辉时间长达20 min.
文摘通过水热法制备Bi2WO6、热分解法制备α-Fe2O3,并利用机械混合的方式获得α-Fe2O3/Bi2WO6复合材料。利用XRD、UV-Vis、BET、SEM、XPS对样品进行表征,相比Bi2WO6,α-Fe2O3/Bi2WO6复合结构在可见光区域的吸收带变宽。在α-Fe2O3/Bi2WO6+H2O2光催化系统中,紫外光照射30 min MO完全降解;模拟太阳光照射60 min MO降解率达到85%,高于单独的Bi2WO6和α-Fe2O3。优良的光催化活性是由于光生电子从α-Fe2O3的导带迁移到Bi2WO6的导带,有效避免了光生电子-空穴的复合,从而提升了光催化效率;在α-Fe2O3/Bi2WO6+H2O2系统中,H2O2作为电子受体,H2O作为空穴受体,能够产生更多的羟基自由基,促进MO降解。
