当前位置: X-MOL 学术Cytotechnology › 论文详情
Our official English website, www.x-mol.net, welcomes your feedback! (Note: you will need to create a separate account there.)
NOL6, a new founding oncogene in human prostate cancer and targeted by miR-590-3p.
Cytotechnology ( IF 2.0 ) Pub Date : 2020-04-05 , DOI: 10.1007/s10616-020-00394-8
Degang Dong 1 , Mei Song 2 , Xiaoli Wu 3 , Wanchun Wang 4
Affiliation  

We identified a new human prostate cancer oncogene, nucleolar protein 6 (NOL6), and screened for microRNAs that interfere with its expression in prostate cancer cells. A NOL6 shRNA plasmid was constructed and packaged into lentivirus to infect PC-3 cells. The ability of cell proliferation was evaluated by cell counting and colony formation. Cell cycle progression and apoptosis of PC-3 cells were detected by flow cytometry. A retrieval database was used to screen possible target microRNAs, and the effect of target miRNA overexpression on PC-3 cells was observed. The results showed that after NOL6 gene knockdown, PC-3 cell mitosis was blocked, proliferation was decreased, and the number of apoptotic cells were increased. The microRNA, hsa-miR-590-3p, that can regulate the NOL6 gene expression was identified. Overexpression of miR-590-3p in PC-3 cells by synthetic mimics resulted in abnormal mitosis, decreased cell proliferation, and an increase in apoptosis. In summary, we identified NOL6 as a novel oncogene in the human prostate cancer PC-3 cell line. The miRNA miR-590-3p interferes with NOL6 expression making it a potential treatment for prostate cancer.

中文翻译:

NOL6是人类前列腺癌中的一个新发现的致癌基因,被miR-590-3p靶向。

我们确定了一种新的人类前列腺癌致癌基因,核仁蛋白6(NOL6),并筛选了干扰其在前列腺癌细胞中表达的microRNA。构建了一个NOL6 shRNA质粒,并将其包装到慢病毒中以感染PC-3细胞。通过细胞计数和集落形成来评估细胞增殖的能力。流式细胞仪检测PC-3细胞的细胞周期进程和凋亡。使用检索数据库筛选可能的靶标microRNA,并观察到靶标miRNA对PC-3细胞的过度表达。结果表明,敲低NOL6基因后,PC-3细胞的有丝分裂被阻断,增殖减少,凋亡细胞数量增加。确定了可调节NOL6基因表达的microRNA hsa-miR-590-3p。合成模拟物在PC-3细胞中过表达miR-590-3p导致异常的有丝分裂,细胞增殖减少和凋亡增加。总之,我们将NOL6鉴定为人类前列腺癌PC-3细胞系中的一种新型致癌基因。miRNA miR-590-3p干扰NOL6表达,使其成为前列腺癌的潜在治疗方法。
更新日期:2020-04-05
down
wechat
bug