Hematologic malignancies are one of the most common cancers,and the incidence has been rising in recent decades.The clinical and molecular features of hematologic malignancies are highly heterogenous,and some hematolo...Hematologic malignancies are one of the most common cancers,and the incidence has been rising in recent decades.The clinical and molecular features of hematologic malignancies are highly heterogenous,and some hematologic malignancies are incurable,challenging the treatment,and prognosis of the patients.However,hematopoiesis and oncogenesis of hematologic malignancies are profoundly affected by epigenetic regulation.Studies have found that methylation-related mutations,abnormal methylation profiles of DNA,and abnormal histone deacetylase expression are recurrent in leukemia and lymphoma.Furthermore,the hypomethylating agents and histone deacetylase inhibitors are effective to treat acute myeloid leukemia and T-cell lymphomas,indicating that epigenetic regulation is indispensable to hematologic oncogenesis.Epigenetic regulation mainly includes DNA modifications,histone modifications,and noncoding RNA-mediated targeting,and regulates various DNA-based processes.This review presents the role of writers,readers,and erasers of DNA methylation and histone methylation,and acetylation in hematologic malignancies.In addition,this review provides the influence of microRNAs and long noncoding RNAs on hematologic malignancies.Furthermore,the implication of epigenetic regulation in targeted treatment is discussed.This review comprehensively presents the change and function of each epigenetic regulator in normal and oncogenic hematopoiesis and provides innovative epigenetic-targeted treatment in clinical practice.展开更多
Targeted regulation of heat transfer in carbon/carbon composite structure is built for cooling electronic device.A three-dimensional data-driven design model coupling genetic algorithm(GA) with self-adaption deep lear...Targeted regulation of heat transfer in carbon/carbon composite structure is built for cooling electronic device.A three-dimensional data-driven design model coupling genetic algorithm(GA) with self-adaption deep learning for targeted regulation of heat transfer in built structure is proposed.The self-adaption deep learning model predicts the temperature of built structure closer to optimal value in GA model.The distributions of pore and carbon fiber bundles in built structure are optimized by the proposed model.The surface temperature of electronic device in the optimized structures is 19.1%-27.5% lower than that in the initial configurations when the porosity of built structure varies from 3% to 11%.The surface temperature of electronic device increases with an increase in porosity.The built structure with carbon fiber bundles near the surface of electronic device and pore distribution in the middle of structure has a higher heat dissipation capacity compared with that in the initial configuration.Besides,the computation time of the proposed model is less than one tenth compared with that of the traditional genetic algorithm.展开更多
[目的]探讨长链非编码RNA MIR4435-2HG(LncRNA MIR4435-2HG)靶向上调转化生长因子-β1(TGF-β1)对非小细胞肺癌(NSCLC)细胞迁移、增殖的作用及其初步机制。[方法]检测NSCLC癌组织及其癌旁组织、NSCLC细胞株及正常人支气管上皮细胞(HBE)...[目的]探讨长链非编码RNA MIR4435-2HG(LncRNA MIR4435-2HG)靶向上调转化生长因子-β1(TGF-β1)对非小细胞肺癌(NSCLC)细胞迁移、增殖的作用及其初步机制。[方法]检测NSCLC癌组织及其癌旁组织、NSCLC细胞株及正常人支气管上皮细胞(HBE)中MIR4435-2HG和TGF-β1表达。将pcDNA-MIR4435-2HG和pcDNA质粒转染至A549细胞,CCK-8法、Transwell法检测细胞增殖、迁移能力。Western Blot法检测细胞TGF-β1表达。免疫共沉淀验证MIR4435-2HG与TGF-β1靶向作用。[结果]NSCLC组织MIR4435-2HG(1.89±0.52 vs 0.76±0.48)和TGF-β1相对表达量(1.43±0.22 vs 0.37±0.18)均高于癌旁组织(P<0.05);与HBE细胞比较,NSCLC细胞株MIR4435-2HG相对表达量升高(P<0.05),且其中A549细胞高于H226细胞(P<0.05);与阴性对照组比较,MIR4435-2HG过表达组细胞MIR4435-2HG(4.72±0.43 vs 3.38±0.46)及TGF-β1(0.82±0.13 vs 1.07±0.24)相对表达量、细胞48 h OD值(0.43±0.03 vs 0.52±0.04)及迁移数量[(89.63±18.28)个vs(169.89±20.34)个]均增加(P<0.05),而与对照组比较,TGF-β1组细胞MIR4435-2HG表达未见显著变化(P>0.05)。[结论] NSCLC组织中MIR4435-2HG呈高表达,LncRNA MIR4435-2HG可能通过靶向上调TGF-β1促进NSCLC细胞迁移和增殖。展开更多
基金This work is supported by the National Natural Science Foundation of China(82204490 to A.Z.)the Translational Research Grant of NCRCH(2021WWB03 to T.N.)+1 种基金Achievement Transformation Project(CGZH21001 to T.N.)1.3.5 Project for Disciplines of Excellence,West China Hospital,Sichuan University(ZYJC21007 to T.N.).
文摘Hematologic malignancies are one of the most common cancers,and the incidence has been rising in recent decades.The clinical and molecular features of hematologic malignancies are highly heterogenous,and some hematologic malignancies are incurable,challenging the treatment,and prognosis of the patients.However,hematopoiesis and oncogenesis of hematologic malignancies are profoundly affected by epigenetic regulation.Studies have found that methylation-related mutations,abnormal methylation profiles of DNA,and abnormal histone deacetylase expression are recurrent in leukemia and lymphoma.Furthermore,the hypomethylating agents and histone deacetylase inhibitors are effective to treat acute myeloid leukemia and T-cell lymphomas,indicating that epigenetic regulation is indispensable to hematologic oncogenesis.Epigenetic regulation mainly includes DNA modifications,histone modifications,and noncoding RNA-mediated targeting,and regulates various DNA-based processes.This review presents the role of writers,readers,and erasers of DNA methylation and histone methylation,and acetylation in hematologic malignancies.In addition,this review provides the influence of microRNAs and long noncoding RNAs on hematologic malignancies.Furthermore,the implication of epigenetic regulation in targeted treatment is discussed.This review comprehensively presents the change and function of each epigenetic regulator in normal and oncogenic hematopoiesis and provides innovative epigenetic-targeted treatment in clinical practice.
基金supported by Guangdong Basic and Applied Basic Research Foundation (2023A1515012297)。
文摘Targeted regulation of heat transfer in carbon/carbon composite structure is built for cooling electronic device.A three-dimensional data-driven design model coupling genetic algorithm(GA) with self-adaption deep learning for targeted regulation of heat transfer in built structure is proposed.The self-adaption deep learning model predicts the temperature of built structure closer to optimal value in GA model.The distributions of pore and carbon fiber bundles in built structure are optimized by the proposed model.The surface temperature of electronic device in the optimized structures is 19.1%-27.5% lower than that in the initial configurations when the porosity of built structure varies from 3% to 11%.The surface temperature of electronic device increases with an increase in porosity.The built structure with carbon fiber bundles near the surface of electronic device and pore distribution in the middle of structure has a higher heat dissipation capacity compared with that in the initial configuration.Besides,the computation time of the proposed model is less than one tenth compared with that of the traditional genetic algorithm.
文摘[目的]探讨长链非编码RNA MIR4435-2HG(LncRNA MIR4435-2HG)靶向上调转化生长因子-β1(TGF-β1)对非小细胞肺癌(NSCLC)细胞迁移、增殖的作用及其初步机制。[方法]检测NSCLC癌组织及其癌旁组织、NSCLC细胞株及正常人支气管上皮细胞(HBE)中MIR4435-2HG和TGF-β1表达。将pcDNA-MIR4435-2HG和pcDNA质粒转染至A549细胞,CCK-8法、Transwell法检测细胞增殖、迁移能力。Western Blot法检测细胞TGF-β1表达。免疫共沉淀验证MIR4435-2HG与TGF-β1靶向作用。[结果]NSCLC组织MIR4435-2HG(1.89±0.52 vs 0.76±0.48)和TGF-β1相对表达量(1.43±0.22 vs 0.37±0.18)均高于癌旁组织(P<0.05);与HBE细胞比较,NSCLC细胞株MIR4435-2HG相对表达量升高(P<0.05),且其中A549细胞高于H226细胞(P<0.05);与阴性对照组比较,MIR4435-2HG过表达组细胞MIR4435-2HG(4.72±0.43 vs 3.38±0.46)及TGF-β1(0.82±0.13 vs 1.07±0.24)相对表达量、细胞48 h OD值(0.43±0.03 vs 0.52±0.04)及迁移数量[(89.63±18.28)个vs(169.89±20.34)个]均增加(P<0.05),而与对照组比较,TGF-β1组细胞MIR4435-2HG表达未见显著变化(P>0.05)。[结论] NSCLC组织中MIR4435-2HG呈高表达,LncRNA MIR4435-2HG可能通过靶向上调TGF-β1促进NSCLC细胞迁移和增殖。
