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首页> 外文期刊>Cancer Cell International >5-alpha-reductase type I (SRD5A1) is up-regulated in non-small cell lung cancer but does not impact proliferation, cell cycle distribution or apoptosis
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5-alpha-reductase type I (SRD5A1) is up-regulated in non-small cell lung cancer but does not impact proliferation, cell cycle distribution or apoptosis

机译：I型5-alpha-还原酶（SRD5A1）在非小细胞肺癌中上调，但不影响增殖，细胞周期分布或凋亡

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Background Non-small cell lung cancer (NSCLC) is one of the most frequent malignancies and has a high mortality rate due to late detection and lack of efficient treatments. Identifying novel drug targets for this indication may open the way for new treatment strategies. Comparison of gene expression profiles of NSCLC and normal adjacent tissue (NAT) allowed to determine that 5-alpha-reductase type I (SRD5A1) was up-regulated in NSCLC compared to NAT. This raised the question whether SRD5A1 was involved in sustained proliferation and survival of NSCLC. Methods siRNA-mediated silencing of SRD5A1 was performed in A549 and NCI-H460 lung cancer cell lines in order to determine the impact on proliferation, on distribution during the different phases of the cell cycle, and on apoptosisecrosis. In addition, lung cancer cell lines were treated with 4-azasteroids, which specifically inhibit SRD5A1 activity, and the effects on proliferation were measured. Statistical analyses using ANOVA and post-hoc Tamhane-T2-test were performed. In the case of non-parametric data, the Kruskal-Wallis test and the post-hoc Mann-Whitney-U-test were used. Results The knock-down of SRDA51 expression was very efficient with the SRD5A1 transcripts being reduced to 10% of control levels. Knock-down efficiency was furthermore confirmed at the protein level. However, no effect of SRD5A1 silencing was observed in the proliferation assay, the cell cycle analysis, and the apoptosisecrosis assay. Treatment of lung cancer cell lines with 4-azasteroids did not significantly inhibit proliferation. Conclusions In summary, the results suggest that SRD5A1 is not a crucial enzyme for the sustained proliferation of NSCLC cell lines.
机译：背景非小细胞肺癌（NSCLC）是最常见的恶性肿瘤之一，由于发现晚和缺乏有效的治疗方法，因此死亡率很高。为这种适应症确定新的药物靶标可能为新的治疗策略开辟道路。比较NSCLC和正常邻近组织（NAT）的基因表达谱，可以确定与NAT相比，NSCLC中的I型5-α-还原酶（SRD5A1）上调了。这就提出了一个问题，即SRD5A1是否参与NSCLC的持续增殖和存活。方法在A549和NCI-H460肺癌细胞系中进行siRNA介导的SRD5A1沉默，以确定对增殖，细胞周期不同阶段的分布以及对细胞凋亡/坏死的影响。另外，用特异性抑制SRD5A1活性的4-氮杂类固醇处理肺癌细胞系，并测量其对增殖的影响。使用ANOVA和事后Tamhane-T2-test进行统计分析。对于非参数数据，使用Kruskal-Wallis检验和事后Mann-Whitney-U检验。结果SRDA51表达的敲除非常有效，SRD5A1转录本降至对照水平的10％。在蛋白水平上进一步证实了敲除效率。但是，在增殖测定，细胞周期分析和凋亡/坏死测定中未观察到SRD5A1沉默的作用。用4-氮杂固醇治疗肺癌细胞系不会显着抑制增殖。结论总而言之，结果表明SRD5A1不是NSCLC细胞系持续增殖的关键酶。

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