Objectives:Glioma,as the most lethal primary brain malignancy with poor prognosis,requires further elucidation on the functional role of long noncoding RNA(lncRNA)DDX11 antisense RNA 1(DDX11-AS1)in its pathogenesis,de...Objectives:Glioma,as the most lethal primary brain malignancy with poor prognosis,requires further elucidation on the functional role of long noncoding RNA(lncRNA)DDX11 antisense RNA 1(DDX11-AS1)in its pathogenesis,despite its established oncogenic functions in other cancers.Therefore,this study sought to characterize the oncogenic role and molecular mechanism of DDX11-AS1 in glioma.Methods:DDX11-AS1 expression levels were analyzed in clinical surgical glioma specimens and publicly available datasets.The functional roles of DDX11-AS1 on glioma cell proliferation and migration were investigated using in vitro knockdown and overexpression assays.In vivo tumor growth was assessed using orthotopic glioma-bearing mouse models.To elucidate the regulatory axis involving DDX11-AS1,miR-1183,and E2F transcription factor 7(E2F7),we performed competitive endogenous RNA(ceRNA)analysis and conducted functional rescue experiments via miR-1183 inhibition.Results:DDX11-AS1 expression was markedly upregulated in clinical glioma specimens.Functionally,DDX11-AS1 knockdown significantly suppressed glioma cell proliferation and migration in vitro,while its overexpression exacerbated these malignant phenotypes.Orthotopic glioma-bearingmouse models confirmed that DDX11-AS1 drives in vivo glioma tumor growth.Mechanistically,DDX11-AS1 functions as a ceRNA by competitively interacting with miR-1183.Critically,inhibition of miR-1183 rescued the suppressive effects of DDX11-AS1 knockdown on glioma tumorigenic phenotypes and restored E2F7 expression levels.Conclusions:This study demonstrates that lncRNA DDX11-AS1 promotes glioma progression by regulating the miR-1183/E2F7 axis,indicating a potential therapeutic target for glioma.展开更多
文摘目的:探究血清补体C1q/肿瘤坏死因子相关蛋白l(complement C1q/tumor necrosis factor-related protein 1,CTRP1)、E2F转录因子2(E2F transcription factor 2,E2F2)、C反应蛋白(C-reaction protein,CRP)水平与急性胰腺炎患者病情程度及预后的相关性。方法:急性胰腺炎患者95例,根据病情分为轻度组61例和重度组34例,以同期健康体检者95例为对照组。比较上述3组及不同预后患者血清CTRP1、E2F2、CRP水平、急性生理学与慢性健康状况评分系统Ⅱ(acute physiology and chronic health evaluation,APACHEⅡ)评分,分析血清CTRP1、E2F2、CRP水平与患者病情程度、预后及APACHEⅡ评分的相关性,血清CTRP1、E2F2、CRP水平对重度急性胰腺炎的诊断价值。结果:重度组血清CTRP1、E2F2、CRP水平及APACHEⅡ评分高于轻度组、对照组,轻度组高于对照组(均P<0.05)。预后不良患者血清CTRP1、E2F2、CRP水平高于预后良好患者(均P<0.001)。血清CTRP1、E2F2、CRP水平与急性胰腺炎患者病情程度、预后及APACHEⅡ评分呈正相关(P<0.001)。血清CTRP1、E2F2、CRP水平联合检测诊断重度急性胰腺炎算曲线下面积(area under curve,AUC)为0.843,敏感度为79.41%,特异度为80.33%,优于CTRP1、E2F2、CRP单项检测。结论:血清CTRP1、E2F2、CRP水平与急性胰腺炎患者病情程度及预后关系密切,联合检测对病情评估及预后预测具有一定价值。
基金supported by Shenzhen Science and Technology Program(JCYJ20220530152614033,JCYJ20230807142213027)Funding Statement Special Fund for Economic and Technological Development in Longgang District,Shenzhen(LGKCYLWS2023028).
文摘Objectives:Glioma,as the most lethal primary brain malignancy with poor prognosis,requires further elucidation on the functional role of long noncoding RNA(lncRNA)DDX11 antisense RNA 1(DDX11-AS1)in its pathogenesis,despite its established oncogenic functions in other cancers.Therefore,this study sought to characterize the oncogenic role and molecular mechanism of DDX11-AS1 in glioma.Methods:DDX11-AS1 expression levels were analyzed in clinical surgical glioma specimens and publicly available datasets.The functional roles of DDX11-AS1 on glioma cell proliferation and migration were investigated using in vitro knockdown and overexpression assays.In vivo tumor growth was assessed using orthotopic glioma-bearing mouse models.To elucidate the regulatory axis involving DDX11-AS1,miR-1183,and E2F transcription factor 7(E2F7),we performed competitive endogenous RNA(ceRNA)analysis and conducted functional rescue experiments via miR-1183 inhibition.Results:DDX11-AS1 expression was markedly upregulated in clinical glioma specimens.Functionally,DDX11-AS1 knockdown significantly suppressed glioma cell proliferation and migration in vitro,while its overexpression exacerbated these malignant phenotypes.Orthotopic glioma-bearingmouse models confirmed that DDX11-AS1 drives in vivo glioma tumor growth.Mechanistically,DDX11-AS1 functions as a ceRNA by competitively interacting with miR-1183.Critically,inhibition of miR-1183 rescued the suppressive effects of DDX11-AS1 knockdown on glioma tumorigenic phenotypes and restored E2F7 expression levels.Conclusions:This study demonstrates that lncRNA DDX11-AS1 promotes glioma progression by regulating the miR-1183/E2F7 axis,indicating a potential therapeutic target for glioma.
