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首页> 外文期刊>Molecular Cancer >BCL11A overexpression predicts survival and relapse in non-small cell lung cancer and is modulated by microRNA-30a and gene amplification
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BCL11A overexpression predicts survival and relapse in non-small cell lung cancer and is modulated by microRNA-30a and gene amplification

机译：BCL11A过表达预测非小细胞肺癌的生存和复发，并受microRNA-30a和基因扩增的调节

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Background Aberrant activation of the proto-oncogene B-cell lymphoma/leukemia 11A ( BCL11A ) has been implicated in the pathogenesis of leukemia and lymphoma. However, the clinical significance of BCL11A in non-small cell lung cancer ( NSCLC ) remains unknown. Results We examined BCL11A expression at the protein and mRNA levels in a cohort (n?=?114) of NSCLC patients and assessed the relationship between BCL11A expression and clinicopathological parameters. Data from array-based Comparative Genomic Hybridization ( aCGH ) and microRNA transfection experiments were integrated to explore the potential mechanisms of abnormal BCL11A activation in NSCLC . Compared to adjacent non-cancerous lung tissues, BCL11A expression levels were specifically upregulated in NSCLC tissues at both the mRNA ( t =?9.81, P 0.001) and protein levels. BCL11A protein levels were higher in patients with squamous histology (χ2?=?15.81, P =?0.001), smokers (χ2?=?8.92, P =?0.004), patients with no lymph node involvement (χ2?=?5.14, P =?0.029), and patients with early stage disease (χ2?=?3.91, P =?0.048). A multivariate analysis demonstrated that in early stage NSCLC (IA–IIB), BCL11A was not only an independent prognostic factor for disease-free survival (hazards ratio [HR] 0.24, 95% confidence interval [CI] 0.12-0.50, P P =?0.003). The average BCL11A expression level was much higher in SCC samples with amplifications than in those without amplifications ( t =?3.30, P =?0.023). Assessing functionality via an in vitro luciferase reporter system and western blotting, we found that the BCL11A protein was a target of miR-30a. Conclusions Our results demonstrated that proto-oncogene BCL11A activation induced by miR-30a and gene amplification may be a potential diagnostic and prognostic biomarker for effective management of this disease.
机译：背景技术原癌基因B细胞淋巴瘤/白血病11A（BCL11A）的异常激活与白血病和淋巴瘤的发病机制有关。然而，BCL11A在非小细胞肺癌（NSCLC）中的临床意义仍然未知。结果我们检查了NSCLC患者队列（n == 114）中蛋白质和mRNA水平的BCL11A表达，并评估了BCL11A表达与临床病理参数之间的关系。整合了来自基于阵列的比较基因组杂交（aCGH）和microRNA转染实验的数据，以探索NSCLC中异常BCL11A激活的潜在机制。与邻近的非癌性肺组织相比，NSCLC组织中BCL11A的表达水平在mRNA水平（t =？9.81，P 0.001）和蛋白质水平均被特异性上调。鳞状组织学（χ 2 ？=？15.81，P =？0.001），吸烟者（χ 2 ？=？8.92，P =？0.004），无淋巴结受累的患者（χ 2 ？=？5.14） ，P =？0.029），以及患有早期疾病的患者（χ 2 ？=？3.91，P =？0.048）。多因素分析表明，在早期NSCLC（IA–IIB）中，BCL11A不仅是无病生存的独立预后因素（危险比[HR] 0.24，95％置信区间[CI] 0.12-0.50，PP =？ 0.003）。具有扩增的SCC样品中的平均BCL11A表达水平比没有扩增的SCC样品中的平均BCL11A表达水平高得多（t =？3.30，P =？0.023）。通过体外荧光素酶报告系统和蛋白质印迹评估功能，我们发现BCL11A蛋白是miR-30a的靶标。结论我们的结果表明，miR-30a诱导的原癌基因BCL11A激活和基因扩增可能是有效控制该疾病的潜在诊断和预后生物标志物。

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