The aim of this study is to analyse the expression status of long non-coding RNA (lncRNA) H19 in nasopharyngeal carcinoma and to unravel its oncogenic properties at molecular level. The abundance of H19, let-7a, b, g, i and HRAS was quantified by real-time PCR. Cell viability was measured by the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide method. Cell proliferation was evaluated by the cell counting. Cell migration and cell invasion were determined using transwell chamber and scattering colony formation. Tumour progression was monitored in xenograft tumour model and tail vein injection was adopted for lung metastasis assessment. Luciferase reporter assay was employed to interrogate the potential regulatory action of let-7 genes on H19 expression. The endogenous HRAS protein was quantified by western blotting. H19 was aberrantly over-expression in nasopharyngeal carcinoma, which intimately associated with poorer prognosis. H19-deficency significantly inhibited cell viability and suppressed cell proliferation. Furthermore, both migrative and invasive capacity were compromised by H19 knockdown. H19-silencing remarkably delayed xenograft tumour progression and lung metastasis. Mechanistically, H19 competitively sponged let-7 genes and therefore up-regulated HRAS, which consequently contributed to its oncogenic activity in nasopharyngeal carcinomas. Our study uncovered the oncogenic properties of H19 in nasopharyngeal carcinoma and highlighted the H19-let-7-HRAS signalling axis underlying the incidence and metastasis of this disease.

中文翻译：

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lncRNA H19的上调以let-7依赖性方式促进鼻咽癌的增殖和转移。

这项研究的目的是分析长非编码RNA（lncRNA）H19在鼻咽癌中的表达状况，并在分子水平上揭示其致癌特性。H19，let-7a，b，g，i和HRAS的丰度通过实时PCR定量。细胞存活力通过3-（4,5-二甲基噻唑-2-基）-2,5-二苯基四氮唑溴化物法测定。通过细胞计数评价细胞增殖。使用transwell室和散射菌落形成来确定细胞迁移和细胞侵袭。在异种移植肿瘤模型中监测肿瘤进展，并采用尾静脉注射进行肺转移评估。萤光素酶报告基因测定被用来询问let-7基因对H19表达的潜在调节作用。内源HRAS蛋白通过蛋白质印迹法定量。H19在鼻咽癌中异常高表达，与预后较差密切相关。H19缺陷显着抑制细胞活力并抑制细胞增殖。此外，H19击倒损害了迁移能力和侵袭能力。H19沉默显着延迟异种移植肿瘤的进展和肺转移。从机制上讲，H19竞争性地吸收了let-7基因，因此上调了HRAS，因此有助于其在鼻咽癌中的致癌活性。我们的研究揭示了H19在鼻咽癌中的致癌特性，并强调了H19-let-7-HRAS信号转导轴是该疾病的发生和转移的基础。H19缺陷显着抑制细胞活力并抑制细胞增殖。此外，H19击倒损害了迁移能力和侵袭能力。H19沉默显着延迟异种移植肿瘤的进展和肺转移。从机制上讲，H19竞争性地吸收了let-7基因，因此上调了HRAS，因此有助于其在鼻咽癌中的致癌活性。我们的研究揭示了H19在鼻咽癌中的致癌特性，并强调了H19-let-7-HRAS信号转导轴是该疾病的发生和转移的基础。H19缺陷显着抑制细胞活力并抑制细胞增殖。此外，H19击倒损害了迁移能力和侵袭能力。H19沉默显着延迟异种移植肿瘤的进展和肺转移。从机制上讲，H19竞争性地吸收了let-7基因，因此上调了HRAS，因此有助于其在鼻咽癌中的致癌活性。我们的研究揭示了鼻咽癌中H19的致癌特性，并强调了H19-let-7-HRAS信号转导轴是这种疾病的发生和转移的基础。H19具有竞争性，可以使let-7基因海绵化，从而上调HRAS，从而有助于其在鼻咽癌中的致癌活性。我们的研究揭示了H19在鼻咽癌中的致癌特性，并强调了H19-let-7-HRAS信号转导轴是该疾病的发生和转移的基础。H19具有竞争性，可以使let-7基因海绵化，从而上调HRAS，从而有助于其在鼻咽癌中的致癌活性。我们的研究揭示了H19在鼻咽癌中的致癌特性，并强调了H19-let-7-HRAS信号转导轴是该疾病的发生和转移的基础。