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首页> 外文期刊>BMC Cancer >LINC01287 facilitates proliferation, migration, invasion and EMT of colon cancer cells via miR-4500/MAP3K13 pathway
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LINC01287 facilitates proliferation, migration, invasion and EMT of colon cancer cells via miR-4500/MAP3K13 pathway

机译:LINC01287通过MIR-4500 / MAP3K13途径促进结肠癌细胞的增殖,迁移,侵袭和EMT

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摘要

Accumulated studies indicate that aberrant expression of long noncoding RNAs (lncRNAs) is associated with tumorigenesis and progression of colon cancer. In the present study, long intergenic non-protein coding RNA 1287 (LINC01287) was identified to up-regulate in colon cancer by transcriptome RNA-sequencing, but the exact function remained unclear. Transcriptome RNA-sequencing was conducted to identify dysregulated lncRNAs. Expression of LINC01287 was evaluated by real-time quantitative PCR. The downstream targets of LINC01287 and miR-4500 were verified by luciferase reporter assay, pull down assay and western blot. The potential functions of LINC01287 were evaluated by cell viability assay, colony formation assay, soft agar assay, flow cytometry, transwell migration and invasion assay, and tumor xenograft growth in colon cancer cells. Our results indicated that LINC01287 was up-regulated in colon cancer patients. High LINC01287 expression was associated with advanced TNM stage, lymph node metastasis, distant metastasis and shorter overall survival. Knockdown of LINC01287 inhibited cell growth, colony formation in plates and soft agar, transwell cell migration and invasion, and epithelial-mesenchymal transition (EMT) of colon cancer cells, while LINC01287 overexpression had contrary effects. In addition, LINC01287 mediated MAP3K13 expression by sponging miR-4500, thus promoted NF-κB p65 phosphorylation. Restored MAP3K13 expression or miR-4500 knockdown partially abrogated the effects of silencing LINC01287 in colon cancer cells. Our findings demonstrated that the LINC01287/miR-4500/MAP3K13 axis promoted progression of colon cancer. Therefore, LINC01287 might be a potential therapeutic target and prognostic marker for colon cancer patients.
机译:积累的研究表明,长度非致rNA(lncrnas)的异常表达与结肠癌的肿瘤引起和进展相关。在本研究中,通过转录组RNA测序鉴定长期非蛋白质编码RNA 1287(LINC01287)在结肠癌中调节,但是确切的功能仍然不清楚。进行转录组RNA测序以鉴定失去剂量的LNCRNA。通过实时定量PCR评估LINC01287的表达。 LINC01287和MIR-4500的下游靶通过Luciferase报道验证,拉下测定和Western印迹。通过细胞活力测定,菌落形成测定,软琼脂测定,流式细胞术,转发迁移和侵袭测定和结肠癌细胞的肿瘤异种移植生长评估LINC01287的潜在功能。我们的研究结果表明,在结肠癌患者中,LINC01287上调。高LINC01287表达与晚期TNM阶段,淋巴结转移,远处转移和较短的整体存活率相关。 LINC01287的敲低抑制细胞生长,菌落形成的平板和软琼脂,Transwell细胞迁移和侵袭,以及结肠癌细胞的上皮 - 间充质转换(EMT),而LINC01287过表达具有相反的作用。此外,LINC01287通过冲水MIR-4500介导的MAP3K13表达,从而促进了NF-κBP65磷酸化。恢复MAP3K13表达或MIR-4500敲除部分废除沉默LINC01287在结肠癌细胞中的影响。我们的研究结果表明,LINC01287 / MIR-4500 / MAP3K13轴促进了结肠癌的进展。因此,LINC01287可能是结肠癌患者的潜在治疗靶标和预后标志物。

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