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长链非编码RNA SOX2OT促进人卵巢癌细胞的增殖和运动。

Long non-coding RNA SOX2OT promotes cell proliferation and motility in human ovarian cancer.

作者信息

Han Ling, Zhang Wei, Zhang Bingyi, Zhan Leyun

机构信息

Department of Obstetrics and Gynecology, Renmin Hospital of Wuhan University, Wuhan, Hubei 430072, P.R. China.

Department of Obstetrics and Gynecology, Renmin Hospital of Three Gorges University, Wuhan, Hubei 430070, P.R. China.

出版信息

Exp Ther Med. 2018 Feb;15(2):2182-2188. doi: 10.3892/etm.2017.5618. Epub 2017 Dec 12.

DOI:10.3892/etm.2017.5618
PMID:29434823
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5776615/
Abstract

Ovarian cancer is one of the most common malignant gynecological cancers. Although conventional chemotherapies have improved the treatment of patients with ovarian cancer, the mortality rate remains high. Hence, it is crucial that the detailed mechanisms that promote ovarian cancer are urgently identified. Therefore, reverse transcription-quantitative polymerase chain reaction was used to reveal the relative transcript levels. Colony formation assay and cell cycle assay were performed in siRNA-treated cells. Transwell assay and western blot assays were also conducted. The results showed that the expression of long non-coding RNA SRY-box 2 overlapping transcript (SOX2OT) was upregulated in clinical ovarian cancer tissues and in cultured ovarian cancer cells (HO-8910 and HO-8910PM). High expression of SOX2OT negatively correlated with the prognosis of patients with ovarian cancer. Knockdown of SOX2OT by specific small interfering RNA against SOX2OT suppressed the colony formation capacity of invasive ovarian cancer cells and resulted in cell cycle arrest in G0/G1 phase. Key cell cycle regulators, cyclin B1 and cell division cycle 25C, were consistently downregulated by the knockdown of SOX2OT. Furthermore, knockdown of SOX2O Tinhibited cell migration, cell invasion and decreased the expression of mesenchymal protein N-cadherin, whereas the expression of epithelial protein E-cadherin was increased in ovarian cancer cells. Overall, SOX2OT expression levels correlated with the prognosis of patients with ovarian cancer, and SOX2OT promoted cell proliferation and motility in ovarian cancer cells. These findings indicated that SOX2OT may serve as a potential therapeutic target in the treatment of ovarian cancer.

摘要

卵巢癌是最常见的妇科恶性肿瘤之一。尽管传统化疗改善了卵巢癌患者的治疗效果,但死亡率仍然很高。因此,迫切需要确定促进卵巢癌发生的详细机制。为此,采用逆转录定量聚合酶链反应来揭示相关转录水平。对经小干扰RNA处理的细胞进行集落形成试验和细胞周期试验。还进行了Transwell试验和蛋白质免疫印迹分析。结果显示,长链非编码RNA SRY盒2重叠转录本(SOX2OT)在临床卵巢癌组织及培养的卵巢癌细胞(HO-8910和HO-8910PM)中表达上调。SOX2OT的高表达与卵巢癌患者的预后呈负相关。用针对SOX2OT的特异性小干扰RNA敲低SOX2OT可抑制侵袭性卵巢癌细胞的集落形成能力,并导致细胞周期停滞于G0/G1期。敲低SOX2OT可使关键细胞周期调节因子细胞周期蛋白B1和细胞分裂周期蛋白25C持续下调。此外,敲低SOX2OT可抑制卵巢癌细胞的迁移、侵袭,并降低间充质蛋白N-钙黏蛋白的表达,而上皮蛋白E-钙黏蛋白的表达则增加。总体而言,SOX2OT表达水平与卵巢癌患者的预后相关,且SOX2OT可促进卵巢癌细胞的增殖和迁移。这些发现表明,SOX2OT可能是治疗卵巢癌的一个潜在治疗靶点。

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Low adherent cancer cell subpopulations are enriched in tumorigenic and metastatic epithelial-to-mesenchymal transition-induced cancer stem-like cells.低粘附性癌细胞亚群富含致瘤性和转移性上皮-间质转化诱导的癌症干细胞样细胞。
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A long noncoding RNA Sox2ot regulates lung cancer cell proliferation and is a prognostic indicator of poor survival.一种长链非编码RNA Sox2ot调控肺癌细胞增殖,是生存预后不良的一个指标。
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Two novel splice variants of SOX2OT, SOX2OT-S1, and SOX2OT-S2 are coupregulated with SOX2 and OCT4 in esophageal squamous cell carcinoma.SOX2OT的两种新型剪接变体,即SOX2OT-S1和SOX2OT-S2,在食管鳞状细胞癌中与SOX2和OCT4共同调控。
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