Long non-coding RNA SNHG10 upregulates BIN1 to suppress the tumorigenesis and epithelial-mesenchymal transition of epithelial ovarian cancer via sponging miR-200a-3p.
Long non-coding RNA SNHG10 upregulates BIN1 to suppress the tumorigenesis and epithelial-mesenchymal transition of epithelial ovarian cancer via sponging miR-200a-3p.
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长非编码RNA SNHG10通过海绵miR-200a-3p上调BIN1抑制上皮性卵巢癌的肿瘤发生和上皮-间质转化
DOI：
10.1038/s41420-022-00825-9
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发表时间：
2022-02-11
影响因子：
7
通讯作者：
Liu L
中科院分区：
文献类型：
--
作者：
Lv W;Jia Y;Wang J;Duan Y;Wang X;Liu T;Hao S;Liu L
上皮性卵巢癌（EOC）是妇科最常见、最致命的恶性肿瘤之一，预后不佳。长链非编码RNA（lncRNA）在上皮性卵巢癌的发生、发展中起着重要作用。然而，参与EOC的lncRNA的谱仍有待扩大，以进一步改善临床治疗策略。在本研究中，我们发现了一个新的肿瘤抑制lncRNA小核仁RNA宿主基因10（SNHG 10）在卵巢癌。Kaplan-Meier分析和考克斯比例风险模型显示SNHG 10低表达与EOC患者预后不良相关。SNHG 10过表达抑制EOC细胞的增殖、集落形成、迁移和侵袭。此外，根据LncBase v.2实验模块，预测SNHG 10在EOC细胞中海绵miR-200 a-3 p。然后，通过进行定量实时PCR（qRT-PCR）和荧光素酶报告基因测定来确认SNHG 10和miR-200 a-3 p的结合。RNA免疫沉淀（RIP）显示SNHG 10和miR-200 a-3 p占据相同的Ago 2蛋白，形成RNA诱导沉默复合物（RISC）。通过重叠来自生物信息学算法的结果，发现肿瘤抑制剂桥接整合子-1（BIN 1）是SNHG 10/miR-200 a-3 p轴的主要下游靶标。免疫组化法检测上皮性卵巢癌组织中BIN 1的低表达。BIN 1和SNHG 10在EOC组织中的表达呈正相关。通过进行miRNA拯救实验，在EOC细胞中验证了SNHG 10/miR-200 a-3 p/BIN 1轴及其对恶性行为和上皮-间质转化（EMT）过程的促进作用。此外，SNHG 10过表达在体内显著抑制EOC细胞的成瘤性和EMT。总之，SNHG 10海绵miR-200 a-3 p上调BIN 1，从而发挥其在EOC中的肿瘤抑制作用。因此，SNHG 10/miR-200 a-3 p/BIN 1轴可能作为治疗EOC的潜在预测生物标志物和治疗靶点。
Epithelial ovarian cancer (EOC) is one of the most frequent and fatal gynecologic malignant tumors resulting in an unsatisfying prognosis. Long non-coding RNAs (lncRNAs) play pivotal roles in the tumorigenesis and progression of EOC. However, the profile of lncRNAs involved in EOC remains to be expanded to further improve clinical treatment strategy. In present study, we identified a novel tumor-suppressive lncRNA small nucleolar RNA host gene 10 (SNHG10) in EOC. Kaplan–Meier analysis and COX proportional hazard progression model showed that low expression of SNHG10 was correlated with a poor prognosis of EOC patients. Overexpressing SNHG10 suppressed the proliferation, colony formation, migration, and invasion of EOC cells. Furthermore, SNHG10 was predicted to sponge miR-200a-3p in EOC cells according to the LncBase v.2 experimental module. Then, the binding of SNHG10 and miR-200a-3p was confirmed by performing quantitative real-time PCR (qRT-PCR) and luciferase reporter assays. RNA immunoprecipitation (RIP) showed that SNHG10 and miR-200a-3p occupied the same Ago2 protein to form an RNA-induced silencing complex (RISC). By overlapping the results from the bioinformatics algorithms, tumor-suppressor bridging integrator-1 (BIN1) was found to be a main downstream target of the SNHG10/miR-200a-3p axis. Low expression of BIN1 in EOC tissues was detected by using immunohistochemistry (IHC). Besides, BIN1 and SNHG10 expression was positively correlated in EOC tissues. By performing miRNA rescue experiments, a SNHG10/miR-200a-3p/BIN1 axis and its promoting effects on malignant behaviors and epithelial–mesenchymal transition (EMT) process were verified in EOC cells. Moreover, SNHG10 overexpression significantly suppressed the tumorigenesis and EMT of EOC cells in vivo. Altogether, SNHG10 sponges miR-200a-3p to upregulate BIN1 and thereby exerting its tumor-suppressive effects in EOC. Therefore, the SNHG10/miR-200a-3p/BIN1 axis may act as a potential predictive biomarker and therapeutic target for treating EOC.
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DOI：
10.1186/s13046-019-1329-2
发表时间：
2019-08-07
影响因子：
11.3
作者：
Long, Xiaoran;Song, Keqi;Di, Wen
通讯作者：
Di, Wen
DOI：
10.1186/s13046-021-01882-1
发表时间：
2021-02-23
期刊：
Journal of experimental & clinical cancer research : CR
影响因子：
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作者：
Si Z;Yu L;Jing H;Wu L;Wang X
通讯作者：
Wang X
影响因子：
16.1
作者：
Khorkova O;Hsiao J;Wahlestedt C
通讯作者：
Wahlestedt C
影响因子：
6.4
作者：
Jia, Yunlong;Wang, Hongyan;Liu, Lihua
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Liu, Lihua
CERNA假设：隐藏RNA语言的Rosetta石头？
影响因子：
64.5
作者：
Salmena L;Poliseno L;Tay Y;Kats L;Pandolfi PP
通讯作者：
Pandolfi PP