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[摘要] 目的:探究lncRNA Linc01296 对卵巢癌细胞顺铂(cisplatin,DDP)抵抗的影响及其作用机制。方法:收集2017 年10月至2018 年10 月四川省人民医院妇科卵巢癌组织样本53 例、交界性卵巢肿瘤样本22 例及良性卵巢肿块组织样本17 例,qPCR检测3 种样本Linc01296 mRNA表达的差异,并分析其与患者临床病理特征的关系。培养人卵巢癌细胞系OVCAR-3(OVCAR-3 Control)及其DDP耐药细胞系(OVCAR-3 DR),慢病毒转染表达靶向Linc01296 siRNA 的载体及对照随机靶向序列载体于OVCAR-3 DR细胞中,作为siLinc01296 和siControl 组,CCK-8 实验检测各组细胞系DDP半抑制浓度(IC50)及耐药指数,qPCR 检测OVCAR-3 Control、DR、DR siControl 及siLinc01296 组细胞系中Linc01296 及肿瘤干细胞相关基因Oct-4 及Sox-2 的mRNA表达水平,WB检测各组细胞系Oct-4 及Sox-2 的蛋白表达水平。结果:OVCAR-3 DR组细胞DDP IC50及耐药指数显著高于OVCAR-3 Control 组(均P<0.01),siLinc01296 组细胞DDP IC50及耐药指数显著低于DR siControl 组(P<0.01),且显著高于OVCAR-3 Control组(P<0.01);DR 组细胞Linc01296、Oct-4 及Sox-2 mRNA 及蛋白表达均高于OVCAR-3 Control 组(均P<0.01),siLinc01296 组Linc01296、Oct-4 及Sox-2 mRNA及蛋白表达显著低于DR siControl 组(均P<0.01),而Oct-4 及Sox-2 mRNA及蛋白均高于OVCAR-3 Control 组(均P<0.01);Linc01296 在卵巢癌组织中的表达显著高于交界性卵巢肿瘤及良性卵巢组织(均P<0.01),且与患者淋巴结转移及临床分期呈正相关(均P<0.05)。结论:Linc01296 可通过提高卵巢癌肿瘤干细胞标志物的表达促进细胞DDP抵抗的发生,且高表达于卵巢癌组织中,与患者病情进展密切相关。  相似文献   
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目的:探究lncRNA01296 在食管癌组织中的表达及其对食管癌TE-2细胞增殖和迁移的影响。方法:收集2017年1 月至2018年9月承德医学院附属医院肿瘤科收治的36例食管癌组织及相应的癌旁组织,并培养人正常食管上皮细胞(HEEC)及人食管癌细胞系ECA109、TE-1 及TE-2。用qPCR检测癌组织及ECA109、TE-1 及TE-2 细胞中lncRNA01296、小核核糖核蛋白A(SNRPA)及神经生长因子(NGF)mRNA的表达水平。重组慢病毒干扰载体转染食管癌细胞系及相应对照细胞系,分别分为干扰1组、干扰2组及对照组,WB实验检测转染后细胞SNRPA 及NGF 蛋白的表达水平,MTS 实验检测转染后TE-2 细胞的增殖能力,Transwell实验检测TE-2 细胞侵袭和迁移能力。结果:lncRNA01296、SNRPA及NGF mRNA在食管癌组织及细胞系中呈高表达(均P<0.01),且lncRNA01296、SNRPA及NGF mRNA在低分化的TE-2细胞中表达高于其他癌细胞(均P<0.05)。干扰1组和干扰2组lncRNA01296、NGF mRNA表达水平明显低于对照组(均P<0.01),而SNRPAmRNA表达水平与对照组无明显差异(P>0.05);干扰1组和干扰2 组SNRPA及NGF蛋白表达水平明显低于对照组(均P<0.01)。敲减48、72 h后,干扰1组及干扰2组TE-2细胞相对增殖能力明显低于对照组(P<0.05或P<0.01);对照组、干扰1组及干扰2组侵袭细胞数分别为(72.0±6.3)、(36.6±4.3)及(33.9±3.7)个,迁移细胞数分别为(85.2±9.9)、(47.5±8.1)及(43.8±6.5)个,干扰1 组及干扰2 组侵袭及迁移细胞数显著低于对照组(均P<0.01);结论:lncRNA01296可通过上调SNRPA表达促进NGF介导的食管癌细胞的增殖和迁移,为临床食管癌诊断和治疗提供新的靶点。  相似文献   
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Background: Recently has been suggested that LINC01296 has an important role in tumor-promoting in different malignancies. We performed first meta-analysis to assess the association between the LINC01296 expression and clinicopathological criteria and the survival of patients with cancers. Methods: Relevant articles Identified by PubMed, EMBASE, Web of Science, and Scopus searching between December 2000 and 28 December 2018. Binomial data were evaluated by the odds ratio (OR) as the rapid statistic. The association between overall survival (OS) and the LINC01296 expression was evaluated using pooling the hazard ratio (HR) with its corresponding 95% confidence interval (CI). Results: Finally, 9 studies with 720 patients with cancer were included. The expression of LINC01296 showed a significant positive association with TNM stage (OR = 2.67, 95% CI = 1.83-3.88), tumor stage (OR= 2.22, 95% CI= 1.34-3.66) and lymph node metastasis (OR = 3.07, 95% CI = 2.23-4.21). A shorter OS was significantly associated with the expression of LINC01296 (HR = 3.95, 95% CI = 2.65-5.25) and lymph node metastasis (HR = 2.39, 95% CI =1.16-3.63). The OS did not show significant association with gender (HR = 0.83, 95% CI = -0.63-2.30) and tumor stage (HR= 2.66, 95% CI= -0.22-5.54). Conclusion: In conclusion, the results of this meta-analysis suggest that the expression of LINC01296 might be considered as a potential biomarker in patients with cancer.  相似文献   
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ObjectiveTo examine the role of the long noncoding RNA LINC01296 in colorectal carcinoma (CRC) and to explore the underlying mechanism.MethodsWe detected LINC01296 expression levels in a cohort of 51 paired CRC and normal tissues. We also assessed the effects of LINC01296 on cell proliferation and apoptosis in CRC cells in vitro, and measured its effect on tumor growth in an in vivo mouse model. We identified the potential downstream targets of LINC01296 and assessed its regulatory effects.ResultsExpression levels of LINC01296 were elevated in 37/51 CRC tissues compared with the corresponding normal tissues and were significantly associated with tumor stage, lymph node metastasis, and distant metastasis. Knockdown of LINC01296 using antisense oligonucleotides inhibited cell proliferation and promoted apoptosis of colon cancer cells in vitro and inhibited tumor growth in vivo. Knockdown of LINC01296 also significantly increased the gene expression of p15 in colon cancer cells. LINC01296-specific suppression of p15 was validated by the interaction between enhancer of zeste homolog 2 and LINC01296.ConclusionOverexpression of LINC01296 suppressed the expression of p15 leading to CRC carcinogenesis. These findings may provide the basis for novel future CRC-targeted therapies.  相似文献   
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