LncRNA SNHG6 Promotes Wilms' Tumor Progression Through Regulating miR-429/FRS2 Axis.

IF 2.4 4区 医学 Q3 MEDICINE, RESEARCH & EXPERIMENTAL
Cancer Biotherapy and Radiopharmaceuticals Pub Date : 2024-05-01 Epub Date: 2021-01-22 DOI:10.1089/cbr.2020.3705
Yingjie Wang, Junli Liu, Qiying Yao, Yuchuan Wang, Zhengjuan Liu, Li Zhang
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引用次数: 0

Abstract

Background: Long noncoding RNA (lncRNA) small nucleolar RNA host gene 6 (SNHG6) has been reported to be an oncogene in a variety of cancers. However, the role of SNHG6 and its associated mechanisms in Wilms' tumor progression remain largely unknown. Methods: The expression of SNHG6, microRNA-429 (miR-429), and FGF receptor substrates 2 (FRS2) messenger RNA (mRNA) was detected by quantitative real-time polymerase chain reaction. Cell proliferation was analyzed through 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and plate colony assay. The apoptosis was assessed by flow cytometry. Cell glycolytic metabolism was analyzed through detecting the lactate dehydrogenase activity, glucose uptake, lactate production, and ATP level. The target relationship between miR-429 and SNHG6 or FRS2 was predicted by miRcode or Starbase and then validated by dual-luciferase reporter assay and RNA pull-down assay. Murine xenograft model was established to validate the function of SNHG6 in vivo. Results: The level of SNHG6 was elevated in Wilms' tumor tissues and cells, and SNHG6 played an oncogenic role to promote the proliferation and glycolysis and restrain the apoptosis of Wilms' tumor cells. MiR-429 was identified as a target of SNHG6, and miR-429 interference partly reversed the inhibitory effects induced by SNHG6 silencing on the malignant behaviors of Wilms' tumor cells. FRS2 mRNA bound to miR-429 in Wilms' tumor cells. SNHG6 upregulated the expression of FRS2 through acting as a sponge of miR-429. MiR-429-induced influences in Wilms' tumor cells were largely counteracted by the overexpression of FRS2. SNHG6 silencing suppressed the Wilms' tumor growth through miR-429/FRS2 axis in vivo. Conclusion: SNHG6 accelerated Wilms' tumor progression through regulating miR-429/FRS2 signaling in vitro and in vivo.

LncRNA SNHG6通过调控miR-429/FRS2轴促进Wilms'肿瘤进展
背景:据报道,长非编码 RNA(lncRNA)小核仁 RNA 宿主基因 6(SNHG6)是多种癌症的致癌基因。然而,SNHG6 在 Wilms 肿瘤进展中的作用及其相关机制在很大程度上仍然未知。研究方法通过实时定量聚合酶链反应检测 SNHG6、microRNA-429(miR-429)和 FGF 受体底物 2(FRS2)信使 RNA(mRNA)的表达。细胞增殖通过 3-(4,5-二甲基噻唑-2-基)-2,5-二苯基溴化四唑(MTT)检测法和平板菌落检测法进行分析。细胞凋亡通过流式细胞术进行评估。通过检测乳酸脱氢酶活性、葡萄糖摄取、乳酸生成和 ATP 水平来分析细胞的糖代谢。通过 miRcode 或 Starbase 预测了 miR-429 与 SNHG6 或 FRS2 之间的靶标关系,然后通过双荧光素酶报告实验和 RNA pull-down 实验进行了验证。建立了小鼠异种移植模型来验证 SNHG6 在体内的功能。结果SNHG6在Wilms'肿瘤组织和细胞中的水平升高,SNHG6具有促进Wilms'肿瘤细胞增殖、糖酵解和抑制凋亡的致癌作用。MiR-429是SNHG6的靶点,干扰miR-429可部分逆转SNHG6沉默对Wilms'肿瘤细胞恶性行为的抑制作用。Wilms 肿瘤细胞中的 FRS2 mRNA 与 miR-429 结合。SNHG6 通过充当 miR-429 的海绵来上调 FRS2 的表达。FRS2的过表达在很大程度上抵消了MiR-429对Wilms'肿瘤细胞的影响。沉默 SNHG6 可通过 miR-429/FRS2 轴抑制 Wilms 肿瘤在体内的生长。结论SNHG6通过调节体外和体内的miR-429/FRS2信号转导加速了Wilms'肿瘤的进展。
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来源期刊
CiteScore
7.80
自引率
2.90%
发文量
87
审稿时长
3 months
期刊介绍: Cancer Biotherapy and Radiopharmaceuticals is the established peer-reviewed journal, with over 25 years of cutting-edge content on innovative therapeutic investigations to ultimately improve cancer management. It is the only journal with the specific focus of cancer biotherapy and is inclusive of monoclonal antibodies, cytokine therapy, cancer gene therapy, cell-based therapies, and other forms of immunotherapies. The Journal includes extensive reporting on advancements in radioimmunotherapy, and the use of radiopharmaceuticals and radiolabeled peptides for the development of new cancer treatments.
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