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The Expression Characteristics,Clinical Relevance and Tumor Inhibition of KCNN3 in Gastric Adenocarcinoma
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作者 ZHAN Zi-Qing JIN Jia-Bei +3 位作者 LI Yu-Xuan SHI Jia-Xin YE Meng JIN Xiao-Feng 《中国生物化学与分子生物学报》 北大核心 2025年第4期560-575,I0003-I0006,共20页
Potassium-calcium activates channel subfamily N member 3(KCNN3/SK3/KCa2.3)is involved in regulating cellular calcium signaling,muscle contraction and neurotransmitter release.Dysregulation of the KCNN3 channel is asso... Potassium-calcium activates channel subfamily N member 3(KCNN3/SK3/KCa2.3)is involved in regulating cellular calcium signaling,muscle contraction and neurotransmitter release.Dysregulation of the KCNN3 channel is associated with the development of various tumors.We use bioinformatics analysis to identify whether KCNN3 regulates the occurrence and development of stomach adenocarcinoma(STAD)as a prognostic target.By analyzing the Human Protein Atlas(HPA)database and The Cancer Genome Atlas(TCGA)database,we found that the protein and mRNA levels of KCNN3 were dramatically reduced in STAD,and TCGA database showed that KCNN3 significantly correlated with the prognosis and clinical features of STAD.In addition,we found that high expression of KCNN3 in STAD reduced the IC 50 of several drugs in STAD cells,suggesting that high expression of KCNN3 correlated with the drug sensitivity of STAD.To investigate the underlying biological mechanism,we identified a potential KCNN3 interaction factor,tumor necrosis factor receptor superfamily member 7(CD27/TNFRSF7),which is expressed at low levels in STAD.RT-qPCR and Western blotting confirmed that KCNN3 and CD27 positively correlated with each other at protein and mRNA levels,and co-immunoprecipitation and immunofluorescence experiments confirmed that the two proteins interact and colocalize in the cytoplasm.Moreover,we confirmed the inhibitory effect of KCNN3 on the proliferation,migration and invasion of human STAD cells in vitro and in vivo through subcutaneous tumorigenesis and cellular experiments.Furthermore,GO/KEGG enrichment analysis showed that KCNN3 was enriched in signaling pathways regulating the immune response and calcium or metal ion transport.Lastly,we verified through cell co-culture,RT-qPCR and CCK8 assays that high expression of KCNN3 can promote the increase of T cell activating factor and the killing effect of T cells on STAD cells.Therefore,our results suggest that KCNN3 is a potential inhibitory factor affecting the occurrence and progression of STAD. 展开更多
关键词 stomach adenocarcinoma(STAD) potassium calcium-activated channel subfamily n member 3(KCnn3/SK3/KCa2.3) tumor necrosis factor receptor superfamily member 7(CD27/TnFRSF7) drug sensitivity bioinformatics analysis
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KCNN4在胰腺癌组织中的表达及其与预后的关系和对胰腺癌细胞增殖的影响
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作者 杨轩 陈昕苑 +2 位作者 阮小玉 吴清如 顾炎 《中国肿瘤生物治疗杂志》 北大核心 2025年第4期371-377,共7页
目的:探究钾钙激活通道亚家族N成员4(KCNN4)在胰腺癌组织中的表达及其对胰腺癌进展的影响,解析KCNN4在胰腺癌临床诊断及预后判断中的作用。方法:利用GEPIA2数据分析平台,结合TCGA和GTEx数据库的数据分析KCNN4在胰腺癌组织中的表达水平... 目的:探究钾钙激活通道亚家族N成员4(KCNN4)在胰腺癌组织中的表达及其对胰腺癌进展的影响,解析KCNN4在胰腺癌临床诊断及预后判断中的作用。方法:利用GEPIA2数据分析平台,结合TCGA和GTEx数据库的数据分析KCNN4在胰腺癌组织中的表达水平及其与患者预后的关系。收集24例海军军医大学长海医院手术切除的胰腺癌患者的癌及癌旁组织标本,通过qPCR、WB法和免疫组化染色技术验证KCNN4在胰腺癌组织中的表达水平。利用shRNA敲低人胰腺癌细胞中BXPC3和PANC-1中KCNN4的表达,通过CCK-8和克隆形成实验检测细胞增殖与生长情况。利用小鼠胰腺癌KPC细胞构建胰腺癌原位成瘤模型,观察敲低KCNN4对胰腺原位成瘤的影响,统计小鼠生存期(OS)。结果:整合TCGA和GTEx数据库数据分析结果发现,KCNN4在胰腺癌组织中高表达(P<0.05),且与患者OS和DFS缩短相关(均P<0.05)。胰腺癌组织中KCNN4 mRNA和蛋白表达量均显著高于癌旁组织(均P<0.01)。KCNN4敲低后,胰腺癌细胞生长速率显著减慢、克隆形成数量显著减少(均P<0.01)。小鼠胰腺原位荷瘤实验结果表明,KCNN4敲低可抑制肿瘤细胞在胰腺原位的生长并延长小鼠OS。结论:KCNN4在胰腺癌组织中高表达,其能促进胰腺癌细胞增殖和胰腺癌进展,与患者预后密切相关,有望作为胰腺癌临床诊断及预后评估的靶点。 展开更多
关键词 胰腺癌 激活通道家族n成员4 增殖 诊断 预后
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