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首页> 外文期刊>Life sciences >LINC00511 knockdown enhances paclitaxel cytotoxicity in breast cancer via regulating miR-29c/CDK6 axis
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LINC00511 knockdown enhances paclitaxel cytotoxicity in breast cancer via regulating miR-29c/CDK6 axis

机译：LINC00511通过调节miR-29c / cdk6轴来抑制乳腺癌中紫杉醇细胞毒性增强紫杉醇细胞毒性

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摘要

Aims: Drug resistance is becoming a major clinical challenge to the success of breast cancer treatment. Compelling evidence has shown the association between the deregulated long non-coding RNAs (lncRNAs) and drug resistance in various malignancies. However, the effects of long intergenic noncoding RNA 00511 (LINC00511), a newly identified oncogenic lncRNA, on the drug resistance of breast cancer cells remain unknown. Main methods: RT-qPCR was performed to detect the expressions of LINC00511, miR-29c, and cyclin dependent kinase 6 (CDK6) in breast cancer tissues and cells. Pearson correlation analysis was used to analyze the correlation between miR-29c, CDK6 and LINC00511 expression in breast cancer tissues. The interactions between LINC00511, CDK6 and miR-29c were explored by luciferase reporter assay, RT-qPCR and western blot. MTT assay and flow cytometry analysis were applied to evaluate paclitaxel cytotoxicity. Key findings: LINC00511 and CDK6 were upregulated while miR-29c was downregulated in breast cancer tissues and cells. miR-29c was negatively correlated with LINC00511 and CDK6 expression while LINC00511 was positively correlated with CDK6 expression in breast cancer tissues. LINC0051 directly interacted with miR-29c to suppress its expression. LINC00511 knockdown enhanced paclitaxel cytotoxicity in breast cancer cells by up-regulating miR-29c. CDK6 was identified as a target of miR-29c. CDK6 knockdown attenuated the effects of miR-29c inhibition on paclitaxel cytotoxicity in breast cancer cells. LINC00511 positively regulated CDK6 expression in breast cancer cells. Significance: LINC00511 knockdown enhanced paclitaxel cytotoxicity in breast cancer cells via regulating miR-29c/CDK6 axis.
机译：目的：耐药性正成为乳腺癌治疗成功的主要临床挑战。令人信服的证据表明，在各种恶性肿瘤中，Dereculated长期非编码RNA（LNCRNA）和耐药性之间的关联。然而，长期非编码RNA 00511（LINC00511），新鉴定的致癌LNCRNA，对乳腺癌细胞的耐药性的影响仍然未知。主要方法：进行RT-QPCR以检测乳腺癌组织和细胞中LINC00511，miR-29c和细胞周期蛋白依赖激酶6（CDK6）的表达。 Pearson相关性分析用于分析MIR-29C，CDK6和LINC00511在乳腺癌组织中表达的相关性。 LINC00511，CDK6和MIR-29C之间的相互作用由荧光素酶报告结果，RT-QPCR和Western印迹探索。施用MTT测定和流式细胞术分析来评估紫杉醇细胞毒性。关键发现：LINC00511和CDK6上调，而MIR-29C在乳腺癌组织和细胞中下调。 miR-29c与LINC00511和CDK6表达呈负相关，而LINC00511与乳腺癌组织中的CDK6表达呈正相关。 LINC0051直接与MIR-29C互动，抑制其表达。 LINC00511通过Up-Consemating MiR-29c敲低乳腺癌细胞中增强的紫杉醇细胞毒性。 CDK6被鉴定为miR-29c的目标。 CDK6敲低抑制miR-29c抑制对乳腺癌细胞紫杉醇细胞毒性的影响。 LINC00511在乳腺癌细胞中积极调节CDK6表达。意义：LINC00511通过调节miR-29c / cdk6轴敲低乳腺癌细胞中紫杉醇细胞毒性的增强型紫杉醇细胞毒性。

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