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首页> 外文期刊>Molecular medicine reports >Long noncoding RNA Lnc-EGFR promotes cell proliferation and inhibits cell apoptosis via regulating the expression of EGFR in human tongue cancer
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Long noncoding RNA Lnc-EGFR promotes cell proliferation and inhibits cell apoptosis via regulating the expression of EGFR in human tongue cancer

机译:长度非编码RNA LNC-EGFR促进细胞增殖,并通过调节人舌癌中EGFR的表达来抑制细胞凋亡

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摘要

Tongue cancer remains a difficult disease to overcome. Long noncoding RNAs (LncRNAs) have been shown to serve significant roles in the diagnosis and treatment of tongue cancer. Herein, the present study aimed to investigate the role of a newly-discovered Lnc, Lnc-EGFR in tongue cancer. The results showed that the transcript level of Lnc-EGFR was upregulated in patients with tongue cancer and in cultured tongue cancer cell lines. Consistently, expression of EGFR was also elevated selectively in cancerous tissues and malignant cell lines. Knockdown of Lnc-EGFR inhibited the clonogenic ability and cell viability of human tongue cancer cell lines UM1 and CAL-27, as evidenced by colony formation assays, and cell proliferation assays. Furthermore, depletion of Lnc-EGFR in UM1 and CAL-27 cells increased cell apoptosis by upregulating the activities of caspase-3, and caspase-9, but not caspase-8. Lnc-EGFR knockdown-mediated inhibition of clonogenic ability and cell viability was rescued by overexpression of EGFR by adding EGFR recombinant protein into both cell lines. Likewise, Lnc-EGFR knockdown-induced cell apoptosis was reversed by co-treatment with recombinant EGFR protein in UM1 and CAL-27 cells. All of these results suggested the oncogenic potential of Lnc-EGFR, which was achieved by positive regulation of EGFR in human tongue cancer.
机译:舌癌仍然是难以克服的困难。已经证明了长时间的NOODING RNA(LNCRNA)在舌癌的诊断和治疗中发挥重要作用。这里,本研究旨在探讨新发现的LNC,LNC-EGFR在舌癌中的作用。结果表明,在舌癌和培养的舌癌细胞系中升高了LNC-EGFR的转录水平。一致地,在癌组织和恶性细胞系中也选择性地升高EGFR的表达。 LNC-EGFR的敲低抑制人舌癌细胞系UM1和CAL-27的克隆能力和细胞活力,如菌落形成测定和细胞增殖测定所证明。此外,UM1和CAL-27细胞中LNC-EGFR的耗尽通过上调Caspase-3和Caspase-9的活性而不是Caspase-8来增加细胞凋亡。通过将EGFR重组蛋白添加到两种细胞系中,通过对EGFR的过表达来抵抗克隆能力和细胞活力的LNC-EGFR敲低介导的抑制。同样地,通过在UM1和CAL-27细胞中的重组EGFR蛋白共同治疗,逆转LNC-EGFR敲低诱导的细胞凋亡。所有这些结果表明LNC-EGFR的致癌潜力,这是通过在人舌癌中的EGFR的正调节来实现的。

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