【摘 要】
：
Though promoting ferroptosis can reduce cisplatin resistance in tumor cells,ferroptosis and cisplatin resistance in bladder urothelial carcinoma(BUC)following long non-coding RNAs(lncRNAs)is largely unknown.Here,we found the highly expressed lncRNA MAF tr
【机 构】
：
Department of Oncology,Third Xiangya Hospital of Central South University,Changsha 410013,China;Depa
论文部分内容阅读
Though promoting ferroptosis can reduce cisplatin resistance in tumor cells,ferroptosis and cisplatin resistance in bladder urothelial carcinoma(BUC)following long non-coding RNAs(lncRNAs)is largely unknown.Here,we found the highly expressed lncRNA MAF transcription factor G antisense RNA 1(MAFG-AS1)in BUC,and its inhibition increased the sensitivity of BUC cells to cisplatin by promoting fer-roptosis.Mechanically,binding to iron chaperone poly(rC)-binding protein 2(PCBP2)facilitated the recruitments of MAFG-AS1 to deubiquitinase ubiquitin carboxyl-terminal hydrolase isozyme L5(UCHL5),thus stabilizing PCBP2 protein itself.Then PCBP2 was confirmed to interact with ferroportin 1(FPN1),an iron export protein,leading to inhibition of ferroptosis.Moreover,the expression of MAFG-AS1 was regulated by the transcriptional factor MAFG.Interestingly,MAFG-AS1 stimulated MAFG transcription by recruiting histone acetyltransferase p300(EP300)to promote the histone 3 at lysine 27(H3K27ac)at genomic locus of MAFG,forming a MAFG-AS1/MAFG positive feedback loop.In patient samples,higher expression of MAFG-AS1 and MAFG in BUC tissues was significantly correlated with T status and N status,such that MAFG-AS1,MAFG,and the combination of the two were indepen-dent prognostic indicators and chemotherapy sensitivity predictive biomarkers for BUC patients.These findings suggest that inhibition of MAFG-AS1 and MAFG can increase the sensitivity of BUC cells to cis-platin through promoting ferroptosis,indicating the novel chemotherapy sensitivity biomarkers and therapeutic target for BUC.
其他文献
Metal-organic framework (MOF) membranes hold great promise in energy-efficient chemical separa-tions.The outstanding challenges of the microstructural design stem from (1) thinning of membranes to immensely reduce the mass-transfer resistance (for high pe
The rate-determining process for sodium storage in TiO2 is greatly depending on charge transfer happen-ing in the electrode materials owing to its inferior diffusion coefficient and electronic conductivity.Apart from reducing the diffusion distance of ion
目的 研究过敏性紫癜(Henoch Sch(o)nlein purpura,HSP)患儿外周血滤泡调节性T细胞(follicular regulatoryT cells,Tfr细胞)、滤泡辅助性T细胞(follicular helperT cells,Tfh细胞)的表达情况,及其与肾脏受累的关系.方法 选取我院2017年2月至2020年3月期间收治的98例HSP患儿为研究组,同时段60例健康体检儿童为对照组.根据患儿肾脏受累情况将研究组分为无肾脏累及组44例(A组)、孤立性血尿组22例(B组)以及血尿合并
目的 探讨N-乙酰半胱氨酸(NAC)对脓毒症肺损伤的作用及机制.方法 48只Balb/c小鼠随机分为对照组、模型组、NAC低剂量组、中剂量组、高剂量组和阳性药组(n=8).给予LPS前1h,腹腔注射药物干预研究.给予LPS 6 h后麻醉,收集肺泡灌洗液(BALF)和血清.苏木精-伊红染色检测肺损伤病理变化;ELISA检测BALF和血清中TNF-α、IL-6和IL-1β含量;Western blot检测组织中NLRP3、Caspase1和ASC蛋白水平;流式细胞术分析M2型巨噬细胞表型;商用试剂盒测量组织中
目的 探讨不同年龄小鼠脾脏B细胞表面免疫球蛋白分子、相关表面分子的表达和功能差异.方法 不同年龄小鼠的脾脏制备成单个核细胞后进行流式细胞术染色,分析B细胞表面分子的表达.纯化CD19+B细胞,用LPS或CpG刺激培养,检测细胞因子和抗体的分泌.结果 小鼠脾脏中的B细胞、浆母细胞和浆细胞数随小鼠年龄增加呈升高趋势,且B细胞表面免疫球蛋白和多种分子的表达也随小鼠年龄的增加而不同.相同刺激条件下,相比新生小鼠,成年小鼠脾脏B细胞产生细胞因子能力较弱,产生抗体能力更强.结论 小鼠脾脏B细胞的表型和功能随年龄的变化
The rational design and construction of novel two-dimensional(2D)carbon nitrides(CNs)beyond g-C3N4 is a hot topic in the fields of chemistry and materials.Inspired by the polymerisation of urea,we have prepared a series of novel C-C bridged heptazine CNs
Flow boiling is an important heat dissipation method for cooling high heat flux surfaces in many indus-trial applications.The heat transfer can be further enhanced by using porous media surfaces due to their high specific surface areas.However,although fl
目的 探讨白介素33 (interleukin 33,IL-33)对单核细胞THP-1的诱导分化作用以及IL-33诱导分化的THP-1对胃癌SGC7901细胞增殖、迁移和侵袭的影响.方法 IL-33刺激THP-1细胞72 h后流式细胞术检测M2巨噬细胞表面分子CD163及CD209的表达;ELISA检测细胞因子IL-10、IL-12、TGF-β、TNF-α的蛋白表达;qRT-PCR检测IL-10、IL-12、TGF-β、TNF-α的mRNA表达.克隆形成实验、细胞迁移侵袭实验检测IL-33刺激后的THP-
目的 研究miR-23基因干扰对风湿性心脏病(rheumatic heart disease,RHD)大鼠心肌纤维化和免疫紊乱的调节与TGF-β的相关性.方法 建立灭活A组β型溶血性链球菌(group A β-hemolytic streptococcus,GSA)诱导的大鼠风湿性心脏病模型.大鼠分为对照组,RHD组(模型组),RHD+inhibitor-NC组(阴性对照组)和RHD+miR-23 inhibitor组(治疗组).采用RT-qPCR检测心肌组织中miR-23表达;HE和Masson染色观察
目的 探讨绞股蓝皂苷(XLIX)调节可溶性T细胞免疫球蛋白和粘蛋白域3(sTim-3)和Tim-3比率在非小细胞肺癌(NSCLC)细胞免疫逃逸中的作用机制.方法 收集临床NSCLC组织,培养A549 NSCLC细胞.使用Tim-3的小干扰RNA重组质粒(siTim-3)和阴性对照(siNC)转染A549细胞;使用5、20、80 μg/ml的XLIX处理A549细胞48 h,A549分别对应的组别为对照组、XLIX-5 μg、XLIX-20 μg、XLIX-80 μg组;MTT法检测细胞增殖活性;Trans