目的:检测miR-34c-3p与增殖细胞核抗原(PCNA)在三阴性乳腺癌(TNBC)组织和血清中的表达,分析二者的相关性,探讨其在TNBC发病中的意义。方法:选择2017年12月至2019年12月于空军军医大学第一附属医院就诊的72例TNBC患者作为实验组(A组),以...目的:检测miR-34c-3p与增殖细胞核抗原(PCNA)在三阴性乳腺癌(TNBC)组织和血清中的表达,分析二者的相关性,探讨其在TNBC发病中的意义。方法:选择2017年12月至2019年12月于空军军医大学第一附属医院就诊的72例TNBC患者作为实验组(A组),以同期就诊的60例乳腺纤维腺瘤或乳腺腺病患者为对照组(B组)。采用Real-time RT-PCR检测乳腺组织标本中miR-34c-3p m RNA及PCNA m RNA的表达;免疫组化检测两组乳腺组织中PCNA蛋白表达;ELISA法检测血清中PCNA的表达。并进一步分析癌组织中miR-34c-3p m RNA的表达与癌组织中PCNA m RNA及血清PCNA水平的相关性。结果:A、B组miR-34c-3p m RNA的相对表达量分别为0.884±0.159及1.255±0.131,A组明显低于B组,差异有统计学意义(P<0.001)。A、B组PCNA m RNA的相对表达量分别为1.544±0.215及1.230±0.204,A组表达高于B组,差异有统计学意义(P<0.001)。免疫组化检测PCNA蛋白表达,A组阳性例数为50例,阴性例数为22例;B组阳性例数为21例,阴性例数为39例;A组阳性率明显高于B组,差异有统计学意义(P<0.001)。两组患者血清中PCNA的表达,A组[(383.194±110.832)pg/ml]明显高于B组[(257.867±101.697)pg/ml],差异有统计学意义(P<0.001)。将A组TNBC患者肿瘤组织miR-34c-3p m RNA表达结果分别与PCNA m RNA表达结果及其血清中PCNA表达结果进行Pearson相关分析,结果显示:miR-34c-3p m RNA与PCNA m RNA及血清PCNA均呈明显负相关关系(P<0.001、P=0.024<0.05)。结论:TNBC组织中miR-34c-3p表达下调,PCNA在癌组织及血清中均表达上调,二者在TNBC患者组织和血清中呈明显负相关关系。miR-34c-3p与PCNA可能在TNBC的发病中起着重要的作用。展开更多
背景:目前已有针对miRNA/mRNA轴调节骨关节炎疾病进程的分子机制研究。先前生物信息学研究发现具有临床预测价值的mRNA(磷脂酶Cδ3:phospholipase C delta 3,PLCD3)及其靶向miRNA(miR-34a-5p),尚缺实验验证其调控骨关节炎的具体作用及...背景:目前已有针对miRNA/mRNA轴调节骨关节炎疾病进程的分子机制研究。先前生物信息学研究发现具有临床预测价值的mRNA(磷脂酶Cδ3:phospholipase C delta 3,PLCD3)及其靶向miRNA(miR-34a-5p),尚缺实验验证其调控骨关节炎的具体作用及机制。目的:探讨miR-34a-5p/PLCD3轴对骨关节炎进展的调控作用及机制。方法:选择15例膝骨关节炎患者的滑膜为骨关节炎组,同时选择同期因创伤致髌骨骨折行内固定术的15例年轻患者的健康滑膜为对照组,Real-time PCR法检测滑膜中PLCD3及miR-34a-5p的表达。通过细胞转染的方法,将人滑膜关节炎成纤维细胞(human fibroblast like synovial cells-osteoarthritis,HFLS-OA)进行处理,并分为miR-34a-5p模拟物组、pCDH-PLCD3组、miR-34a-5p模拟物+pCDH-PLCD3组、miR-34a-5p抑制剂组、si-PLCD3组、miR-34a-5p抑制剂+si-PLCD3组,通过Real-time PCR法检测PLCD3和miR-34a-5p表达的关系;通过CCK-8法、细胞划痕实验检测各组HFLS-OA细胞活力及细胞迁移的影响;使用Western Blot法检测凋亡标记蛋白表达水平;使用ELISA法检测炎症因子的表达。结果与结论:①PLCD3是miR-34a-5p的直接靶标,同时PLCD3和miR-34a-5p表达水平呈负相关。②PLCD3上调会促进HFLS-OA细胞的增殖并抑制细胞迁移,而miR-34a-5p上调会显著抑制HFLS-OA细胞的活性并增强细胞迁移;miR-34a-5p过表达使HFLS-OA细胞Casp3和Casp9蛋白水平显著升高,而PLCD3过表达则表现出相反趋势。③PLCD3过表达显著增加了HFLS-OA细胞白细胞介素6和肿瘤坏死因子α的表达,而miR-34a-5p模拟物则表现出保护活性。④结果说明,miR-34a-5p/PLCD3轴可能通过调节滑膜细胞的炎症过程或凋亡来影响骨关节炎的进展。展开更多
Background:Renalfibrosis is an important process in the development of chronic kidney disease.Understanding the pathogenesis andfinding effective treatments for renalfibrosis is crucial.This study aims to investigate whe...Background:Renalfibrosis is an important process in the development of chronic kidney disease.Understanding the pathogenesis andfinding effective treatments for renalfibrosis is crucial.This study aims to investigate whether a newly discovered long non-coding RNA(lncRNA)called LOC103694972 could be a potential target for treatingfibrosis of NRK-49F cells.Methods:LncRNA Chip was used to identify differentially expressed lncRNAs between TGF-β1-induced NRK-49F cells and normal cells.The dual-luciferase assay confirmed the binding between miR-29c-3p and signal transducer and activator of transcription(STAT3),as well as between miR-29c-3p and lncRNA LOC103694972.Si-LOC103694972 and miR-29c-3p mimic were then transfected into TGF-β1-induced NRK-49F cells.Results:The study found that LOC103694972 was highly expressed in TGF-β1-induced NRK-49F cells.These cells exhibited increased cell length and activity compared to the control group.The expression levels of Collagen I,α-Smooth muscle actin(α-SMA),and tissue inhibitor of metalloproteinase(TIMP-1)were increased,while matrix Metalloproteinase 2(MMP2)and matrix Metalloproteinase 9(MMP9)expression was decreased.However,transfection with si-LOC103694972 and miR-29c-3p mimics restored cell morphology and reduced cell viability.This led to a decrease in the levels of Collagen I,α-SMA,and TIMP-1,as well as an increase in MMP2 and MMP9 expression.Additionally,TGF-β1-induced NRK-49F cells transfected with miR-29c-3p mimics activated the STAT3-Smad3/CTGF pathway.Conclusion:Based on thesefindings,lncRNA LOC103694972 shows promise as a target for treating renalfibrosis.It negatively regulates miR-29c-3p and activates the STAT3-Smad3/CTGF pathway.展开更多
文摘目的:检测miR-34c-3p与增殖细胞核抗原(PCNA)在三阴性乳腺癌(TNBC)组织和血清中的表达,分析二者的相关性,探讨其在TNBC发病中的意义。方法:选择2017年12月至2019年12月于空军军医大学第一附属医院就诊的72例TNBC患者作为实验组(A组),以同期就诊的60例乳腺纤维腺瘤或乳腺腺病患者为对照组(B组)。采用Real-time RT-PCR检测乳腺组织标本中miR-34c-3p m RNA及PCNA m RNA的表达;免疫组化检测两组乳腺组织中PCNA蛋白表达;ELISA法检测血清中PCNA的表达。并进一步分析癌组织中miR-34c-3p m RNA的表达与癌组织中PCNA m RNA及血清PCNA水平的相关性。结果:A、B组miR-34c-3p m RNA的相对表达量分别为0.884±0.159及1.255±0.131,A组明显低于B组,差异有统计学意义(P<0.001)。A、B组PCNA m RNA的相对表达量分别为1.544±0.215及1.230±0.204,A组表达高于B组,差异有统计学意义(P<0.001)。免疫组化检测PCNA蛋白表达,A组阳性例数为50例,阴性例数为22例;B组阳性例数为21例,阴性例数为39例;A组阳性率明显高于B组,差异有统计学意义(P<0.001)。两组患者血清中PCNA的表达,A组[(383.194±110.832)pg/ml]明显高于B组[(257.867±101.697)pg/ml],差异有统计学意义(P<0.001)。将A组TNBC患者肿瘤组织miR-34c-3p m RNA表达结果分别与PCNA m RNA表达结果及其血清中PCNA表达结果进行Pearson相关分析,结果显示:miR-34c-3p m RNA与PCNA m RNA及血清PCNA均呈明显负相关关系(P<0.001、P=0.024<0.05)。结论:TNBC组织中miR-34c-3p表达下调,PCNA在癌组织及血清中均表达上调,二者在TNBC患者组织和血清中呈明显负相关关系。miR-34c-3p与PCNA可能在TNBC的发病中起着重要的作用。
基金This work was supported by the Hunan Provincial Education Department General Project Research Fund(No.20C1412)the Hunan Graduate Scientific Research Innovation Project(No.CX2018B474)the National Famous Elderly Chinese Medicine Experts Xinyu Chen Inheritance Workshop Construction Project(No.[2022]75).
文摘Background:Renalfibrosis is an important process in the development of chronic kidney disease.Understanding the pathogenesis andfinding effective treatments for renalfibrosis is crucial.This study aims to investigate whether a newly discovered long non-coding RNA(lncRNA)called LOC103694972 could be a potential target for treatingfibrosis of NRK-49F cells.Methods:LncRNA Chip was used to identify differentially expressed lncRNAs between TGF-β1-induced NRK-49F cells and normal cells.The dual-luciferase assay confirmed the binding between miR-29c-3p and signal transducer and activator of transcription(STAT3),as well as between miR-29c-3p and lncRNA LOC103694972.Si-LOC103694972 and miR-29c-3p mimic were then transfected into TGF-β1-induced NRK-49F cells.Results:The study found that LOC103694972 was highly expressed in TGF-β1-induced NRK-49F cells.These cells exhibited increased cell length and activity compared to the control group.The expression levels of Collagen I,α-Smooth muscle actin(α-SMA),and tissue inhibitor of metalloproteinase(TIMP-1)were increased,while matrix Metalloproteinase 2(MMP2)and matrix Metalloproteinase 9(MMP9)expression was decreased.However,transfection with si-LOC103694972 and miR-29c-3p mimics restored cell morphology and reduced cell viability.This led to a decrease in the levels of Collagen I,α-SMA,and TIMP-1,as well as an increase in MMP2 and MMP9 expression.Additionally,TGF-β1-induced NRK-49F cells transfected with miR-29c-3p mimics activated the STAT3-Smad3/CTGF pathway.Conclusion:Based on thesefindings,lncRNA LOC103694972 shows promise as a target for treating renalfibrosis.It negatively regulates miR-29c-3p and activates the STAT3-Smad3/CTGF pathway.
