BACKGROUND The treatment of gastric cancer(GC)has caused an enormous social burden worldwide.Accumulating studies have reported that N6-methyladenosine(m6A)is closely related to tumor progression.METTL5 is a m6A methy...BACKGROUND The treatment of gastric cancer(GC)has caused an enormous social burden worldwide.Accumulating studies have reported that N6-methyladenosine(m6A)is closely related to tumor progression.METTL5 is a m6A methyltransferase that plays a pivotal role in maintaining the metabolic stability of cells.However,its aberrant regulation in GC has not been fully elucidated.AIM To excavate the role of METTL5 in the development of GC.METHODS METTL5 expression and clinicopathological characteristics were analyzed via The Cancer Genome Atlas dataset and further verified via immunohistochemistry,western blotting and real-time quantitative polymerase chain reaction in tissue microarrays and clinical samples.The tumor-promoting effect of METTL5 on HGC-27 and AGS cells was explored in vitro by Cell Counting Kit-8 assays,colony formation assays,scratch healing assays,transwell assays and flow cytometry.The tumor-promoting role of METTL5 in vivo was evaluated in a xenograft tumor model.The EpiQuik m6A RNA Methylation Quantification Kit was used for m6A quantification.Next,liquid chromatography-mass spectrometry was used to evaluate the association between METTL5 and sphingomyelin metabolism,which was confirmed by Enzyme-linked immunosorbent assay and rescue tests.In addition,we investigated whether METTL5 affects the sensitivity of GC cells to cisplatin via colony formation and transwell experiments.RESULTS Our research revealed substantial upregulation of METTL5,which suggested a poor prognosis of GC patients.Increased METTL5 expression indicated distant lymph node metastasis,advanced cancer stage and pathological grade.An increased level of METTL5 correlated with a high degree of m6A methylation.METTL5 markedly promotes the proliferation,migration,and invasion of GC cells in vitro.METTL5 also promotes the growth of GC in animal models.METTL5 knockdown resulted in significant changes in sphingomyelin metabolism,which implies that METTL5 may impact the development of GC via sphingomyelin metabolism.In addition,high METTL5 expression led to cisplatin resistance.CONCLUSION METTL5 was found to be an oncogenic driver of GC and may be a new target for therapy since it facilitates GC carcinogenesis through sphingomyelin metabolism and cisplatin resistance.展开更多
支持等式测试的标识加密(identity-based encryption with equality test, IBEET)体制解决了传统等式测试方案中证书管理的问题,得到了广泛的关注.但现有的IBEET体制难以抵抗渗透攻击,且都是基于国外密码算法设计,不具有自主知识产权....支持等式测试的标识加密(identity-based encryption with equality test, IBEET)体制解决了传统等式测试方案中证书管理的问题,得到了广泛的关注.但现有的IBEET体制难以抵抗渗透攻击,且都是基于国外密码算法设计,不具有自主知识产权.基于此,提出一种支持等式测试并具有密码逆向防火墙的SM9标识加密方案(SM9 identity-based encryption scheme with equality test and cryptographic reverse firewalls, SM9-IBEET-CRF).该方案在用户与云服务器的上行信道间部署密码逆向防火墙(cryptographic reverse firewalls,CRF),对用户发出的信息执行重随机化以达到抵抗渗透攻击的作用.该方案拓展国密算法SM9至IBEET领域中,提升其运行效率并丰富国密算法在云计算领域的研究.给出了SM9-IBEET-CRF的形式化定义和安全模型,并在随机预言机模型中考虑2种不同的敌手将此方案在选择密文攻击下的不可区分性与单向性分别形式化地规约到BDH困难假设上.同时,该方案通过考虑第3种敌手证明CRF的部署为其带来维持功能性、保留安全性以及抵抗渗透性.实验仿真和分析结果展示了该方案的有效性.展开更多
文摘BACKGROUND The treatment of gastric cancer(GC)has caused an enormous social burden worldwide.Accumulating studies have reported that N6-methyladenosine(m6A)is closely related to tumor progression.METTL5 is a m6A methyltransferase that plays a pivotal role in maintaining the metabolic stability of cells.However,its aberrant regulation in GC has not been fully elucidated.AIM To excavate the role of METTL5 in the development of GC.METHODS METTL5 expression and clinicopathological characteristics were analyzed via The Cancer Genome Atlas dataset and further verified via immunohistochemistry,western blotting and real-time quantitative polymerase chain reaction in tissue microarrays and clinical samples.The tumor-promoting effect of METTL5 on HGC-27 and AGS cells was explored in vitro by Cell Counting Kit-8 assays,colony formation assays,scratch healing assays,transwell assays and flow cytometry.The tumor-promoting role of METTL5 in vivo was evaluated in a xenograft tumor model.The EpiQuik m6A RNA Methylation Quantification Kit was used for m6A quantification.Next,liquid chromatography-mass spectrometry was used to evaluate the association between METTL5 and sphingomyelin metabolism,which was confirmed by Enzyme-linked immunosorbent assay and rescue tests.In addition,we investigated whether METTL5 affects the sensitivity of GC cells to cisplatin via colony formation and transwell experiments.RESULTS Our research revealed substantial upregulation of METTL5,which suggested a poor prognosis of GC patients.Increased METTL5 expression indicated distant lymph node metastasis,advanced cancer stage and pathological grade.An increased level of METTL5 correlated with a high degree of m6A methylation.METTL5 markedly promotes the proliferation,migration,and invasion of GC cells in vitro.METTL5 also promotes the growth of GC in animal models.METTL5 knockdown resulted in significant changes in sphingomyelin metabolism,which implies that METTL5 may impact the development of GC via sphingomyelin metabolism.In addition,high METTL5 expression led to cisplatin resistance.CONCLUSION METTL5 was found to be an oncogenic driver of GC and may be a new target for therapy since it facilitates GC carcinogenesis through sphingomyelin metabolism and cisplatin resistance.
文摘支持等式测试的标识加密(identity-based encryption with equality test, IBEET)体制解决了传统等式测试方案中证书管理的问题,得到了广泛的关注.但现有的IBEET体制难以抵抗渗透攻击,且都是基于国外密码算法设计,不具有自主知识产权.基于此,提出一种支持等式测试并具有密码逆向防火墙的SM9标识加密方案(SM9 identity-based encryption scheme with equality test and cryptographic reverse firewalls, SM9-IBEET-CRF).该方案在用户与云服务器的上行信道间部署密码逆向防火墙(cryptographic reverse firewalls,CRF),对用户发出的信息执行重随机化以达到抵抗渗透攻击的作用.该方案拓展国密算法SM9至IBEET领域中,提升其运行效率并丰富国密算法在云计算领域的研究.给出了SM9-IBEET-CRF的形式化定义和安全模型,并在随机预言机模型中考虑2种不同的敌手将此方案在选择密文攻击下的不可区分性与单向性分别形式化地规约到BDH困难假设上.同时,该方案通过考虑第3种敌手证明CRF的部署为其带来维持功能性、保留安全性以及抵抗渗透性.实验仿真和分析结果展示了该方案的有效性.
