超声引导下肝癌穿刺组织中DEK表达的临床意义

为探讨超声引导下穿刺活检肝癌组织中DEK表达的临床意义,作者利用36例经超声引导下穿刺所得的肝癌组织经免疫组化方法检测DEK蛋白的表达,得出结果：肝穿癌组织DEK阳性表达率为52.8%（17/36）,明显高于癌旁正常肝组织（阳性率为0%,0/8）（p=0.007）,与肿块大小密切相关（p=0.040）。结果表明,DEK与肝癌的发生发展有一定关系,超声引导下肝肿物穿刺活检并检测肿瘤组织中相关基因的表达对肝癌治疗有一定的指导价值。     

The m6A Methyltransferase METTL3-Mediated N6-Methyladenosine Modification of DEK mRNA to Promote Gastric Cancer Cell Growth and Metastasis

Gastric cancer (GC) is the fifth most common cancer and the third deadliest cancer in the world, and the occurrence and development of GC are influenced by epigenetics. Methyltransferase-like 3 (METTL3) is a prominent RNA n6-adenosine methyltransferase (m6A) that plays an important role in tumor growth by controlling the work of RNA. This study aimed to reveal the biological function and molecular mechanism of METTL3 in GC. The expression level of METTL3 in GC tissues and cells was detected by qPCR, Western blot and immunohistochemistry, and the expression level and prognosis of METTL3 were predicted in public databases. CCK-8, colony formation, transwell and wound healing assays were used to study the effect of METTL3 on GC cell proliferation and migration. In addition, the enrichment effect of METTL3 on DEK mRNA was detected by the RIP experiment, the m6A modification effect of METTL3 on DEK was verified by the MeRIP experiment and the mRNA half-life of DEK when METTL3 was overexpressed was detected. The dot blot assay detects m6A modification at the mRNA level. The effect of METTL3 on cell migration ability in vivo was examined by tail vein injection of luciferase-labeled cells. The experimental results showed that METTL3 was highly expressed in GC tissues and cells, and the high expression of METTL3 was associated with a poor prognosis. In addition, the m6A modification level of mRNA was higher in GC tissues and GC cell lines. Overexpression of METTL3 in MGC80-3 cells and AGS promoted cell proliferation and migration, while the knockdown of METTL3 inhibited cell proliferation and migration. The results of in vitro rescue experiments showed that the knockdown of DEK reversed the promoting effects of METTL3 on cell proliferation and migration. In vivo experiments showed that the knockdown of DEK reversed the increase in lung metastases caused by the overexpression of METTL3 in mice. Mechanistically, the results of the RIP experiment showed that METTL3 could enrich DEK mRNA, and the results of the MePIP and RNA half-life experiments indicated that METTL3 binds to the 3’UTR of DEK, participates in the m6A modification of DEK and promotes the stability of DEK mRNA. Ultimately, we concluded that METTL3 promotes GC cell proliferation and migration by stabilizing DEK mRNA expression. Therefore, METTL3 is a potential biomarker for GC prognosis and a therapeutic target.     

鞍山某磁选铁精矿阳离子反浮选试验

以六偏磷酸钠、苛性淀粉为调整剂,DEK为新型阳离子反浮选捕收剂,对鞍山某铁矿选矿厂磁选铁精矿进行了反浮选工艺研究。结果表明,以DEK为核心的阳离子反浮选药剂体系与原阴离子反浮选药剂体系相比,药剂制度明显简化,可在中性环境下浮选,浮选无需蒸汽加温至30 ℃左右;采用试验确定的流程和药剂制度处理该磁选铁精矿,可获得铁品位为66.02%、回收率为90.16%的最终铁精矿。     

超声引导下肝癌穿刺组织中DEK表达的临床意义

为探讨超声引导下穿刺活检肝癌组织中DEK表达的临床意义,作者利用36例经超声引导下穿刺所得的肝癌组织经免疫组化方法检测DEK蛋白的表达,得出结果:肝穿癌组织DEK阳性表达率为52.8%(17/36),明显高于癌旁正常肝组织(阳性率为0%,0/8)(p=0.007),与肿块大小密切相关(p=0.040).结果表明,DEK...     

Long Non-Coding LEF1-AS1 Sponge miR-5100 Regulates Apoptosis and Autophagy in Gastric Cancer Cells via the miR-5100/DEK/AMPK-mTOR Axis

DEK and miR-5100 play critical roles in many steps of cancer initiation and progression and are directly or indirectly regulated by most promoters and repressors. LEF1-AS1 as a long non-coding RNA can regulate tumor development through sponge miRNA. The effect and regulatory mechanism of DEK on autophagy and apoptosis in gastric cancer (GC), and the role between miR-5100 and DEK or miR-5100 and LEF1-AS1 are still unclear. Our study found that DEK was highly expressed in gastric cancer tissues and cell lines, and knockdown of DEK inhibited the autophagy of cells, promoted apoptosis, and suppressed the malignant phenotype of gastric cancer. DEK regulates autophagy and apoptosis through the AMPK/mTOR signaling pathway. In addition, miR-5100 inhibits autophagy and promotes apoptosis in GC cells while LEF1-AS1 had the opposite effect. Studies have shown that miR-5100 acts by targeting the 3′UTR of DEK, and LEF1-AS1 regulates the expression of miR-5100 by sponging with mIR-5100. In conclusion, our results found that LEF1-AS1 and miR-5100 sponge function, and the miR-5100/DEK/AMPK/mTOR axis regulates autophagy and apoptosis in gastric cancer cells.     

癌基因DEK蛋白表达判断肺鳞状细胞癌预后的临床价值

为了探讨癌基因DEK蛋白在肺鳞癌中的表达及预后评估价值,应用免疫组化染色检测96例肺鳞癌及其癌旁正常组织中DEK蛋白的表达,结合临床生物学指标及生存时间进行统计学分析。结果发现,肺鳞癌组织中DEK蛋白阳性表达率为45.83%,明显高于癌旁正常组织（15.73%,P=0.001）,DEK蛋白在肺鳞癌中的表达与肿瘤大小（P=0.008）、组织分化程度（P=0.004）及病理学分期（P=0.011）密切相关;癌组织中DEK蛋白的阳性率与患者总生存期明显相关,且与病理分期、CEA水平和转移共同影响患者预后;DEK是肺鳞癌不良预后的独立风险因子。得出结论：检测肺鳞癌组织中DEK蛋白的表达对其预后有一定的临床评估价值,有望成为肺鳞癌新的预后生物标志物。