Downregulated Long Noncoding RNA PART1 Inhibits Proliferation and Promotes Apoptosis in Bladder Cancer (Publication with Expression of Concern. See vol. 21, 2022)

Downregulated Long Noncoding RNA PART1 Inhibits Proliferation and Promotes Apoptosis in Bladder Cancer (Publication with Expression of Concern. See vol. 21, 2022)
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下调长链非编码 RNA PART1 抑制膀胱癌增殖并促进细胞凋亡

DOI:
10.1177/1533033819846638
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发表时间:
2019-07-16
影响因子:
2.8
通讯作者:
Hu, Xiaowen
Hu, Xiaowen
中科院分区:
医学4区
文献类型:
--
作者:
Hu, Xin;Feng, Hefei;Hu, Xiaowen

文献摘要

被引文献

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目的:本研究旨在探讨长链非编码核糖核酸前列腺素调节转录本-1对膀胱癌细胞增殖和凋亡的影响。研究方法:采用基因芯片技术研究膀胱癌组织(N = 9)和非癌膀胱组织(N = 5)中长链非编码核糖核酸的表达谱。通过实时定量逆转录-聚合酶链反应检测组织样本或细胞系中的相对前列腺雄激素调节转录本-1表达水平。pcDNA3.1-prostrate androgen-regulated transcript-1转染后prostrate androgen-regulated transcript-1表达增强,pcMV-sh-prostrate androgen-regulated transcript-1感染后表达下调。另外,细胞增殖和凋亡分别通过细胞计数试剂盒-8分析和流式细胞术测量。通过Transwell测定确定细胞侵袭。结果:前列腺雄激素调节转录本-1在膀胱癌组织中的表达高于癌旁组织。在膀胱癌细胞系(5637,T24)中,前列腺雄激素调节转录本-1的表达被pcDNA3.1-prostrate androgen-regulated transcript-1上调,而被pCMV-sh-prostrate androgen-regulated transcript-1消减。前列腺雄激素调节转录本-1表达增强可促进细胞增殖和侵袭,抑制细胞凋亡。然而,前列腺雄激素调节转录本-1表达的敲低抑制细胞增殖和侵袭,并诱导细胞凋亡。结论:总之,这些数据表明,前列腺雄激素调节的转录本-1的敲低代表了膀胱癌中的肿瘤抑制因子,并有助于抑制肿瘤增殖,促进细胞凋亡和抑制细胞侵袭。前列腺激素调节转录本-1可能作为一种新的预后生物标志物和膀胱癌患者的一个可行的治疗靶点。
Objective: In this study, we aimed to clarify the effects of long noncoding ribonucleic acid prostrate androgen-regulated transcript-1 on bladder cancer cell proliferation and apoptosis. Methods: Microarrays were implemented to investigate the long noncoding ribonucleic acid expression profiles in bladder cancer tissue (N = 9) and in noncancer bladder tissue (N = 5). Relative prostrate androgen-regulated transcript-1 expression levels in tissue samples or cell lines were detected by real-time quantitative reverse transcription-polymerase chain reaction. Prostrate androgen-regulated transcript-1 expression was enhanced by the transfection of pcDNA3.1-prostrate androgen-regulated transcript-1 and downregulated by the infection with pcMV-sh prostrate androgen-regulated transcript-1. Additionally, cell proliferation and apoptosis were measured by the cell counting kit-8 assay and flow cytometry, respectively. Cell invasion was determined by a Transwell assay. Results: Prostrate androgen-regulated transcript-1 expression was upregulated in bladder cancer tissues compared to adjacent nontumor tissues. Furthermore, prostrate androgen-regulated transcript-1 levels were successfully upregulated by pcDNA3.1-prostrate androgen-regulated transcript-1 and depleted by pCMV-sh prostrate androgen-regulated transcript-1 in bladder cancer cell lines (5637, T24). Enhanced prostrate androgen-regulated transcript-1 expression promoted cell proliferation and invasion and inhibited cell apoptosis. However, knockdown of prostrate androgen-regulated transcript-1 expression inhibited cell proliferation and invasion and induced cell apoptosis. Conclusion: In summary, these data suggest that the knockdown of prostrate androgen-regulated transcript-1 represents a tumor suppressor player in bladder cancer and contributes to the inhibition of tumor proliferation, the promotion of cell apoptosis, and the suppression of cell invasion. Prostrate androgen-regulated transcript-1 may function as a new prognostic biomarker and as a feasible therapeutic target for patients with bladder cancer.