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The MicroRNA hsa-let-7g Promotes Proliferation and Inhibits Apoptosis in Lung Cancer by Targeting HOXB1.

MicroRNA hsa-let-7g通过靶向hoxb1 促进肺癌的增殖和抑制细胞凋亡。

  • 影响因子:0
  • DOI:10.3349/ymj.2020.61.3.210
  • 作者列表:"Cui F","Zhou Q","Xiao K","Ma S
  • 发表时间:2020-03-01
Abstract

PURPOSE:The goal of this study was to explore the effects of hsa-let-7g on cell proliferation and apoptosis, and elucidate its role in lung cancer development. MATERIALS AND METHODS:The expression levels of has-let-7g and HOXB1 in tissues and cells were measured by qRT-PCR. An inhibitor of hsa-let-7g or one targeting a control messenger RNA were transfected into A549 and H1944 lung cancer cells, and the effects of hsa-let-7g dysregulation on cell viability and apoptosis were analyzed using CCK-8 and apoptosis detection assays. HOXB1 was confirmed as the target gene of hsa-let-7g, based on luciferase reporter assay results. The relationship between hsa-let-7g and HOXB1 was confirmed by co-transfection of inhibitors of hsa-let-7g and HOXB1 followed by Western blot, CCK-8, and apoptosis detection assays. RESULTS:We observed high expression of hsa-let-7g in lung cancer tissues compared to the corresponding normal tissues, and generally higher expression of hsa-let-7g in patients with advanced tumor classification. The results of CCK-8 and apoptosis detection experiments showed that the inhibition of hsa-let-7g significantly inhibited proliferation of A549 and H1944 cells, but also promoted apoptosis. HOXB1 is a specific target of hsa-let-7g, and downregulation of HOXB1 in lung cancer cells reversed the suppressive effects caused by knocking down hsa-let-7g. CONCLUSION:These data collectively suggest that the expression of hsa-let-7g inhibits lung cancer cells apoptosis and promotes proliferation by down-regulating HOXB1. The results from this study demonstrate the potential of hsa-let-7g/HOXB1 axis as a therapeutic target for the treatment of lung cancer.

摘要

目的: 探讨hsa-let-7g对肺癌细胞增殖和凋亡的影响,阐明其在肺癌发生发展中的作用。 材料和方法: 通过qRT-PCR检测组织和细胞中has-let-7g和HOXB1 的表达水平。将hsa-let-7g或一种靶向对照信使RNA的抑制剂转染到A549 和H1944 肺癌细胞中,使用hsa-let-7g和细胞凋亡检测分析CCK-8 失调对细胞活力和细胞凋亡的影响。基于荧光素酶报告基因测定结果,确定HOXB1 为hsa-let-7g的靶基因。通过hsa-let-7g和HOXB1 的抑制剂的共转染,随后通过蛋白质印迹、hsa-let-7g和细胞凋亡检测试验证实CCK-8 和HOXB1 之间的关系。 结果: 与相应的正常组织相比,我们在肺癌组织中观察到hsa-let-7g的高表达,并且在晚期肿瘤分类的患者中普遍高表达hsa-let-7g。CCK-8 和凋亡检测实验结果表明,抑制hsa-let-7g能显著抑制A549 和H1944 细胞的增殖,同时也促进细胞凋亡。HOXB1 是hsa-let-7g的特异性靶点,肺癌细胞中HOXB1 的下调逆转了敲低hsa-let-7g引起的抑制作用。 结论: 这些数据共同表明hsa-let-7g的表达通过下调hoxb1 抑制肺癌细胞凋亡和促进增殖。该研究的结果证明了hsa-let-7g/HOXB1 轴作为治疗肺癌的治疗靶标的潜力。

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影响因子:6.93
发表时间:2020-01-15
DOI:10.1002/ijc.32532
作者列表:["Hata A","Nakajima T","Matsusaka K","Fukuyo M","Morimoto J","Yamamoto T","Sakairi Y","Rahmutulla B","Ota S","Wada H","Suzuki H","Matsubara H","Yoshino I","Kaneda A"]

METHODS::Patients with idiopathic pulmonary fibrosis (IPF) have higher risk of developing lung cancer, for example, squamous cell carcinoma (SCC), and show poor prognosis, while the molecular basis has not been fully investigated. Here we conducted DNA methylome analysis of lung SCC using 20 SCC samples with/without IPF, and noncancerous lung tissue samples from smokers/nonsmokers, using Infinium HumanMethylation 450K array. SCC was clustered into low- and high-methylation epigenotypes by hierarchical clustering analysis. Genes hypermethylated in SCC significantly included genes targeted by polycomb repressive complex in embryonic stem cells, and genes associated with Gene Ontology terms, for example, "transcription" and "cell adhesion," while genes hypermethylated specifically in high-methylation subgroup significantly included genes associated with "negative regulation of growth." Low-methylation subgroup significantly correlated with IPF (78%, vs. 17% in high-methylation subgroup, p = 0.04), and the correlation was validated by additional Infinium analysis of SCC samples (n = 44 in total), and data from The Cancer Genome Atlas (n = 390). The correlation between low-methylation subgroup and IPF was further validated by quantitative methylation analysis of marker genes commonly hypermethylated in SCC (HOXA2, HOXA9 and PCDHGB6), and markers specifically hypermethylated in high-methylation subgroup (DLEC1, CFTR, MT1M, CRIP3 and ALDH7A1) in 77 SCC cases using pyrosequencing (p = 0.003). Furthermore, low-methylation epigenotype significantly correlated with poorer prognosis among all SCC patients, or among patients without IPF. Multivariate analysis showed that low-methylation epigenotype is an independent predictor of poor prognosis. These may suggest that lung SCC could be stratified into molecular subtypes with distinct prognosis, and low-methylation lung SCC that significantly correlates with IPF shows unfavorable outcome.

翻译标题与摘要 下载文献
影响因子:6.93
发表时间:2020-01-01
DOI:10.1002/ijc.32530
作者列表:["Zhang L","Yang Y","Chai L","Bu H","Yang Y","Huang H","Ran J","Zhu Y","Li L","Chen F","Li W"]

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肺肿瘤方向

肺肿瘤,又叫支气管肺癌,是常见的恶性肿瘤之一。肺肿瘤的治疗为包括手术、中药、放疗、化疗及免疫等多学科的综合治疗。

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