BACKGROUND A series of long non-coding RNAs(lncRNAs)have been reported to play a crucial role in cancer biology.Some previous studies report that lncRNA CDKN2B-AS1 is involved in some human malignancies.However,its ro...BACKGROUND A series of long non-coding RNAs(lncRNAs)have been reported to play a crucial role in cancer biology.Some previous studies report that lncRNA CDKN2B-AS1 is involved in some human malignancies.However,its role in hepatocellular carcinoma(HCC)has not been fully deciphered.AIM To decipher the role of CDKN2B-AS1 in the progression of HCC.METHODS CDKN2B-AS1 expression in HCC was detected by quantitative real-time polymerase chain reaction.The malignant phenotypes of Li-7 and SNU-182 cells were detected by the CCK-8 method,EdU method,and flow cytometry,respectively.RNA immunoprecipitation was executed to confirm the interaction between CDKN2B-AS1 and E2F transcription factor 1(E2F1).Luciferase reporter assay and chromatin immunoprecipitation were performed to verify the binding of E2F1 to the promoter of G protein subunit alpha Z(GNAZ).E2F1 and GNAZ were detected by western blot in HCC cells.RESULTS In HCC tissues,CDKN2B-AS1 was upregulated.Depletion of CDKN2B-AS1 inhibited the proliferation of HCC cells,and the depletion of CDKN2B-AS1 also induced cell cycle arrest and apoptosis.CDKN2B-AS1 could interact with E2F1.Depletion of CDKN2B-AS1 inhibited the binding of E2F1 to the GNAZ promoter region.Overexpression of E2F1 reversed the biological effects of depletion of CDKN2B-AS1 on the malignant behaviors of HCC cells.CONCLUSION CDKN2B-AS1 recruits E2F1 to facilitate GNAZ transcription to promote HCC progression.展开更多
据Sen L 2025年7月11日[Sci Adv,2025,11(28):eads4371-eads4371.]报道,瑞典卡罗林斯卡研究所、法国蒙多尔生物医学研究所和荷兰因兰特大学的研究人员发现了一种称为TMEM9B-AS1的分子,是一种长链非编码RNA(lncRNA),在调节细胞功能中发...据Sen L 2025年7月11日[Sci Adv,2025,11(28):eads4371-eads4371.]报道,瑞典卡罗林斯卡研究所、法国蒙多尔生物医学研究所和荷兰因兰特大学的研究人员发现了一种称为TMEM9B-AS1的分子,是一种长链非编码RNA(lncRNA),在调节细胞功能中发挥重要作用。这一发现可能解释了为什么2型糖尿病患者经常出现肌肉无力和肌肉流失这一影响生活质量和整体健康的原因。展开更多
目的探讨长链非编码RNA(lncRNA)NUTM2B-AS1在口腔鳞状细胞癌组织中的表达及对口腔鳞状细胞癌细胞侵袭和迁移的影响及分子机制。方法采用癌症基因组图谱(The Cancer Genome Atlas,TCGA)数据库分析口腔鳞状细胞癌组织和癌旁组织中NUTM2B-...目的探讨长链非编码RNA(lncRNA)NUTM2B-AS1在口腔鳞状细胞癌组织中的表达及对口腔鳞状细胞癌细胞侵袭和迁移的影响及分子机制。方法采用癌症基因组图谱(The Cancer Genome Atlas,TCGA)数据库分析口腔鳞状细胞癌组织和癌旁组织中NUTM2B-AS1表达水平。qRT-PCR法检测口腔上皮角质细胞HOK、口腔鳞状细胞癌细胞系Cal-27、SCC-25、SCC-9、HSC-3中NUTM2B-AS1表达水平。Cal-27细胞分别转染NUTM2B-AS1过表达载体(pmirGLO-NUTM2B-AS1)和空载体(pmirGLO),记为NUTM2B-AS1组和对照组,qRT-PCR验证每组细胞中NUTM2B-AS1表达水平。Transwell侵袭实验和细胞划痕实验检测Cal-27细胞侵袭和迁移。生物信息学方法和双荧光素酶报告基因实验验证NUTM2B-AS1和miR-770-5p的靶向关系。qRT-PCR检测Cal-27细胞miR-770-5p的表达,Western blot检测Cal-27细胞Sirt7/Smad4信号通路蛋白(Sirt7、E-cadherin、Smad4、MMP-7、Vimentin)的表达。结果与癌旁组织比较,口腔鳞状细胞癌组织中NUTM2B-AS1表达显著降低(P<0.01)。与HOK细胞比较,口腔鳞状细胞癌细胞系Cal-27、SCC-25、SCC-9、HSC-3中NUTM2B-AS1表达显著降低(P<0.01),Cal-27细胞中NUTM2B-AS1表达最低(P<0.01)。与对照组比较,NUTM2B-AS1组Cal-27细胞中NUTM2B-AS1表达显著升高(P<0.01)。与对照组比较,NUTM2B-AS1组Cal-27细胞侵袭数显著降低(P<0.01),Cal-27细胞划痕愈合率显著降低(P<0.01)。miR-770-5p是NUTM2B-AS1的靶向结合基因(P<0.01)。与对照组相比,NUTM2B-AS1组Cal-27细胞中miR-770-5p表达显著降低(P<0.01),Sirt7、E-cadherin蛋白表达显著升高(P<0.01),Smad4、MMP-7、Vimentin蛋白表达下降(P<0.01)。结论NUTM2B-AS1在口腔鳞状细胞癌组织和细胞系中低表达,高表达NUTM2B-AS1可抑制口腔鳞状细胞癌细胞侵袭和迁移,其作用机制与靶向下调miR-770-5p表达有关。展开更多
目的:研究代谢综合征(MS)痰证人群不同症候群形成与CDKAL1、CDKN2A多态性及m RNA表达的关系。方法:收集236例MS患者,采用证素辨证方法分为痰证与非痰证组,并根据2005年国际糖尿病联盟诊断标准,将痰证组患者分为A、B、C和D4个不同症候群...目的:研究代谢综合征(MS)痰证人群不同症候群形成与CDKAL1、CDKN2A多态性及m RNA表达的关系。方法:收集236例MS患者,采用证素辨证方法分为痰证与非痰证组,并根据2005年国际糖尿病联盟诊断标准,将痰证组患者分为A、B、C和D4个不同症候群组,同时选取150名健康人群作为对照。采用SNPscanTM多重SNP分型技术进行CDKAL1 rs10946398及CDKN2A rs10811661基因分型,Real-time PCR检测其m RNA的表达。结果:D组及非痰证组的CDKAL1 rs10946398位点CC、CA基因型及等位基因C的比例较痰证A组显著升高(P<0.05,P<0.01)。痰证组CDKAL1及CDKN2A m RNA表达水平较健康组及非痰证组显著升高(P<0.01,P<0.05),非痰证组CDKAL1 m RNA表达水平较健康组升高(P<0.01);痰证D组CDKAL1 m RNA表达水平较痰证A组显著升高(P<0.01)。结论:携带CDKAL1 rs10946398等位基因C可导致MS痰证中心性肥胖、糖脂代谢紊乱及高血压症候群的产生,其相应的CDKAL1 m RNA表达量也显著升高。CDKN2A m RNA与MS痰证的形成具有一定相关性,其在MS痰证各症候群中表达量一致。展开更多
文摘BACKGROUND A series of long non-coding RNAs(lncRNAs)have been reported to play a crucial role in cancer biology.Some previous studies report that lncRNA CDKN2B-AS1 is involved in some human malignancies.However,its role in hepatocellular carcinoma(HCC)has not been fully deciphered.AIM To decipher the role of CDKN2B-AS1 in the progression of HCC.METHODS CDKN2B-AS1 expression in HCC was detected by quantitative real-time polymerase chain reaction.The malignant phenotypes of Li-7 and SNU-182 cells were detected by the CCK-8 method,EdU method,and flow cytometry,respectively.RNA immunoprecipitation was executed to confirm the interaction between CDKN2B-AS1 and E2F transcription factor 1(E2F1).Luciferase reporter assay and chromatin immunoprecipitation were performed to verify the binding of E2F1 to the promoter of G protein subunit alpha Z(GNAZ).E2F1 and GNAZ were detected by western blot in HCC cells.RESULTS In HCC tissues,CDKN2B-AS1 was upregulated.Depletion of CDKN2B-AS1 inhibited the proliferation of HCC cells,and the depletion of CDKN2B-AS1 also induced cell cycle arrest and apoptosis.CDKN2B-AS1 could interact with E2F1.Depletion of CDKN2B-AS1 inhibited the binding of E2F1 to the GNAZ promoter region.Overexpression of E2F1 reversed the biological effects of depletion of CDKN2B-AS1 on the malignant behaviors of HCC cells.CONCLUSION CDKN2B-AS1 recruits E2F1 to facilitate GNAZ transcription to promote HCC progression.
文摘据Sen L 2025年7月11日[Sci Adv,2025,11(28):eads4371-eads4371.]报道,瑞典卡罗林斯卡研究所、法国蒙多尔生物医学研究所和荷兰因兰特大学的研究人员发现了一种称为TMEM9B-AS1的分子,是一种长链非编码RNA(lncRNA),在调节细胞功能中发挥重要作用。这一发现可能解释了为什么2型糖尿病患者经常出现肌肉无力和肌肉流失这一影响生活质量和整体健康的原因。
文摘目的探讨长链非编码RNA(lncRNA)NUTM2B-AS1在口腔鳞状细胞癌组织中的表达及对口腔鳞状细胞癌细胞侵袭和迁移的影响及分子机制。方法采用癌症基因组图谱(The Cancer Genome Atlas,TCGA)数据库分析口腔鳞状细胞癌组织和癌旁组织中NUTM2B-AS1表达水平。qRT-PCR法检测口腔上皮角质细胞HOK、口腔鳞状细胞癌细胞系Cal-27、SCC-25、SCC-9、HSC-3中NUTM2B-AS1表达水平。Cal-27细胞分别转染NUTM2B-AS1过表达载体(pmirGLO-NUTM2B-AS1)和空载体(pmirGLO),记为NUTM2B-AS1组和对照组,qRT-PCR验证每组细胞中NUTM2B-AS1表达水平。Transwell侵袭实验和细胞划痕实验检测Cal-27细胞侵袭和迁移。生物信息学方法和双荧光素酶报告基因实验验证NUTM2B-AS1和miR-770-5p的靶向关系。qRT-PCR检测Cal-27细胞miR-770-5p的表达,Western blot检测Cal-27细胞Sirt7/Smad4信号通路蛋白(Sirt7、E-cadherin、Smad4、MMP-7、Vimentin)的表达。结果与癌旁组织比较,口腔鳞状细胞癌组织中NUTM2B-AS1表达显著降低(P<0.01)。与HOK细胞比较,口腔鳞状细胞癌细胞系Cal-27、SCC-25、SCC-9、HSC-3中NUTM2B-AS1表达显著降低(P<0.01),Cal-27细胞中NUTM2B-AS1表达最低(P<0.01)。与对照组比较,NUTM2B-AS1组Cal-27细胞中NUTM2B-AS1表达显著升高(P<0.01)。与对照组比较,NUTM2B-AS1组Cal-27细胞侵袭数显著降低(P<0.01),Cal-27细胞划痕愈合率显著降低(P<0.01)。miR-770-5p是NUTM2B-AS1的靶向结合基因(P<0.01)。与对照组相比,NUTM2B-AS1组Cal-27细胞中miR-770-5p表达显著降低(P<0.01),Sirt7、E-cadherin蛋白表达显著升高(P<0.01),Smad4、MMP-7、Vimentin蛋白表达下降(P<0.01)。结论NUTM2B-AS1在口腔鳞状细胞癌组织和细胞系中低表达,高表达NUTM2B-AS1可抑制口腔鳞状细胞癌细胞侵袭和迁移,其作用机制与靶向下调miR-770-5p表达有关。
文摘目的:研究代谢综合征(MS)痰证人群不同症候群形成与CDKAL1、CDKN2A多态性及m RNA表达的关系。方法:收集236例MS患者,采用证素辨证方法分为痰证与非痰证组,并根据2005年国际糖尿病联盟诊断标准,将痰证组患者分为A、B、C和D4个不同症候群组,同时选取150名健康人群作为对照。采用SNPscanTM多重SNP分型技术进行CDKAL1 rs10946398及CDKN2A rs10811661基因分型,Real-time PCR检测其m RNA的表达。结果:D组及非痰证组的CDKAL1 rs10946398位点CC、CA基因型及等位基因C的比例较痰证A组显著升高(P<0.05,P<0.01)。痰证组CDKAL1及CDKN2A m RNA表达水平较健康组及非痰证组显著升高(P<0.01,P<0.05),非痰证组CDKAL1 m RNA表达水平较健康组升高(P<0.01);痰证D组CDKAL1 m RNA表达水平较痰证A组显著升高(P<0.01)。结论:携带CDKAL1 rs10946398等位基因C可导致MS痰证中心性肥胖、糖脂代谢紊乱及高血压症候群的产生,其相应的CDKAL1 m RNA表达量也显著升高。CDKN2A m RNA与MS痰证的形成具有一定相关性,其在MS痰证各症候群中表达量一致。
