Long non-coding RNA DPP10-AS1 represses the proliferation and invasiveness of glioblastoma by regulating miR-24-3p/CHD5 signaling pathway

This investigation aimed to unveil new prospective diagnosis-related biomarkers together with treatment targets against glioblastoma.Methods:The expression levels of long non-coding RNA(lncRNA)DPP10-AS1 were assessed using real-time quantitative polymerase chain reaction(RT-qPCR)within both the patient tissue specimens and glioblastoma cell lines.The relationship between lncRNA DPP10-AS1 expression in glioblastoma and patient prognosis was investigated.Cell Counting Kit-8(CCK-8),transwell,and clonogenic experiments were utilized to assess tumor cells’proliferation,invasiveness,and migratory potentials after lncRNA DPP10-AS1 expression was up or down-regulated.Using an online bioinformatics prediction tool,the intracellular localization of lncRNA DPP10-AS1 and its target miRNA were predicted,and RNA-FISH verified results.A dual-luciferase reporter experiment validated the relationship across miR-24-3p together with lncRNA DPP10-AS1.MiR-24-3p expression within glioblastoma was identified through RT-qPCR,and potential link across miR-24-3p and lncRNA DPP10-AS1 was assessed using Pearson correlation analysis.Moreover,influence from lncRNA DPP10-AS1/miR-24-3p axis upon glioblastoma cell progression was assessed in vivo via a subcutaneous xenograft tumor model.Results:The expression of lncRNA DPP10-AS1 was notably reduced in both surgical specimens of glioblastoma and the equivalent cell lines.Low level of lncRNA DPP10-AS1 in glioblastoma is following poor prognosis.The downregulation of lncRNA DPP10-AS1 in glioblastoma cells resulted in enhanced cellular proliferation,migration,and invasion capabilities,accompanied by downregulated E-cadherin and upregulated vimentin and N-cadherin.Additionally,the observed upregulation of lncRNA DPP10-AS1 demonstrated a substantial inhibitory function upon proliferation,invasion,and migratory capabilities of LN229 cells.Subcellular localization disclosed that lncRNA DPP10-AS1 had a binding site that interacted with miR-24-3p.Upregulated miR-24-3p was detected in glioblastomas,displaying an inverse correlation with lncRNA DPP10-AS1 expression.MiR-24-3p downstream target has been determined as chromodomain helicase DNA binding protein 5(CHD5).LncRNA DPP10-AS1 affected the invasion and proliferation of glioblastoma by controlling the miR-24-3p/CHD5 axis.Conclusion:The present study demonstrated that lncRNA DPP10-AS1 can inhibit the invasive,migratory,and proliferative properties of glioblastoma by regulating the miR-24-3p/CHD5 signaling pathway.Consequently,lncRNA DPP10-AS1 has potential as a tumor suppressor and might be utilized for accurate diagnosis and targeted treatments of glioblastomas.

LncRNA DPP10-AS1 promotes malignant processes through epigenetically activating its cognate gene DPP10 and predicts poor prognosis in lung cancer patients

Objective:The purpose of this study was to explore the function and gene expression regulation of the newly identified lnc RNA DPP10-AS1 in lung cancer,and its potential value as a prognostic biomarker.Methods:q RT-PCR and Western blot were conducted to detect the expression of DDP10-AS1 and DPP10 in lung cancer cell lines and tissues.The effects of DDP10-AS1 on DPP10 expression,cell growth,invasion,apoptosis,and in vivo tumor growth were investigated in lung cancer cells by Western blot,rescue experiments,colony formation,flow cytometry,and xenograft animal experiments.Results:The novel antisense lnc RNA DPP10-AS1 was found to be highly expressed in cancer tissues(P<0.0001),and its upregulation predicted poor prognosis in patients with lung cancer(P=0.0025).Notably,DPP10-AS1 promoted lung cancer cell growth,colony formation,and cell cycle progression,and repressed apoptosis in lung cancer cells by upregulating DPP10 expression.Additionally,DPP10-AS1 facilitated lung tumor growth via upregulation of DPP10 protein in a xenograft mouse model.Importantly,DPP10-AS1 positively regulated DPP10 gene expression,and both were coordinately upregulated in lung cancer tissues.Mechanically,DPP10-AS1 was found to associate with DPP10 m RNA but did not enhance DPP10 m RNA stability.Hypomethylation of DPP10-AS1 and DPP10 contributed to their coordinate upregulation in lung cancer.Conclusions:These findings indicated that the upregulation of the antisense lnc RNA DPP10-AS1 promotes lung cancer malignant processes and facilitates tumorigenesis by epigenetically regulating its cognate sense gene DPP10.DPP10-AS1 may serve as a candidate prognostic biomarker and a potential therapeutic target in lung cancer.

LOC389023在难治性颞叶癫痫中分子海绵机制的预测

【目的】研究可能与LOC389023和二肽基肽酶10(DPP10)作用的micro RNA在难治性颞叶癫痫患者皮质中的表达变化,预测LOC389023在颞叶癫痫中的分子海绵机制。【方法】15例脑外伤患者切除的皮质为正常组,26例难治性颞叶癫痫患者行癫痫灶切除的皮质为癫痫组。运用western blot、免疫组织化学染色检测DPP10和电压依赖性钾通道4.3(Kv4.3)的表达变化,采用免疫荧光染色对DPP10和kv4.3进行定位,采用免疫共沉淀分析DPP10与Kv4.3的相关性。运用miRanda、Pita、Target Scan和miRDB软件分别预测与LOC389023以及DPP10相互作用的micro RNA。采用q PCR技术检测LOC389023以及micro RNA的表达变化。【结果】免疫组织化学染色和western blot分析结果显示,DPP10在癫痫组中高表达(P<0.05),Kv4.3则低表达(P<0.05);DPP10与Kv4.3共表达于神经元的细胞膜且两者有相互作用;通过软件预测得到5个候选micro RNA(miR-32-5p,miR-140-5p,miR-367-3p,miR-25-3p和miR-4325);q PCR检测结果显示:在癫痫组中,LOC389023和miR-140-5p表达水平均低于对照组(P<0.05),miR-25-3p和miR-367-3p表达水平均高于对照组(P<0.05),而miR-32-5p和miR-4325无明显变化(P>0.05)。【结论】LOC389023可能以分子海绵的机制调控miR-25-3p和miR-367-3p,继而调控DPP10的表达参与癫痫的形成。