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首页> 外文期刊>RSC Advances >Long non-coding RNA NEAT1 accelerates cell progression in cervical cancer by regulating the miR-889-3p/E2F7 axis through the activation of the PI3K/AKT pathway
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Long non-coding RNA NEAT1 accelerates cell progression in cervical cancer by regulating the miR-889-3p/E2F7 axis through the activation of the PI3K/AKT pathway

机译：通过激活PI3K / AKT途径来调节miR-889-3P / E2F7轴，长期非编码RNA Neat1加速宫颈癌的细胞进展

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Cervical cancer (CC) is a common malignant gynecological cancer that is frequently diagnosed in women. Apparently, long noncoding RNA nuclear-enriched autosomal transcript 1 (NEAT1) has been identified as a tumor promoter in multiple cancers. Our research is focused on the effects of lncRNA NEAT1 on cell progression in cervical cancer and the potential molecular mechanism of NEAT1 for CC cell progression. The levels of NEAT1, MicroRNA (miR)-889-3p and E2F transcription factor 7 (E2F7) in CC tumors and cells were measured by a quantitative real-time polymerase chain reaction (qRT-PCR). The interaction of miR-889-3p with NEAT1 and E2F7 was validated by a luciferase reporter system and a RNA immunoprecipitation (RIP) assay, respectively. Cell counting kit-8 (CCK-8) and flow cytometry were used for cell proliferation and apoptosis evaluation. Cell migration and invasion were examined by a transwell assay. The protein expressions of E2F7, AKT, phospho-AKT (p-AKT), phosphatidylinositol 3-kinase (PI3K) and phosphorylated PI3K (p-PI3K) were analyzed by western blot assay. Animal models were established by subcutaneously injecting the Me180 cells stably transfected with sh-NEAT1 and sh-NC. The expressions of NEAT1 and E2F7 were up-regulated, whereas the expression of miR-889-3p was down-regulated in the CC tumors and cells when compared with those in normal tumors and cells. The interaction between miR-889-3p and NEAT1 or E2F7 was proved by luciferase reporter system and RIP assay. In addition, the miR-889-3p inhibitor attenuated the NEAT1 silencing-induced inhibition effects on cell proliferation, migration, and invasion and the promotion effects on apoptosis in CC. Consistently, E2F7 reversed the miR-889-3p-mediated inhibition on cell progression in CC. Moreover, NEAT1 modulated cell behavior by targeting the miR-889-3p/E2F7 axis through the PI3K/AKT pathway. Finally, the intervention of NEAT1 hindered tumor growth in vivo. Thus, NEAT1 contributes to cell progression in CC by targeting miR-889-3p to facilitate the E2F7 expression through the activation of the PI3K/AKT pathway, representing an alternative targeted therapy of CC.
机译：宫颈癌（CC）是一种常见的恶性妇科癌症，其经常被诊断为女性。显然，已经鉴定了长时间的NOTCODINGRNA核富集的常规转录1（NEAT1）作为多种癌症中的肿瘤启动子。我们的研究专注于LNCrNA Neat1对宫颈癌细胞进展的影响及术语CC细胞进展的潜在分子机制。通过定量的实时聚合酶链反应（QRT-PCR）测量CC肿瘤和细胞中的Neat1，microRNA（MIR）-889-3P和E2F转录因子7（E2F7）的水平。 MiR-889-3P与Neat1和E2F7的相互作用分别通过荧光素酶报告系统和RNA免疫沉淀（RIP）测定验证。电池计数试剂盒-8（CCK-8）和流式细胞术用于细胞增殖和凋亡评估。通过Transwell测定检查细胞迁移和侵袭。通过蛋白质印迹测定分析E2F7，AKT，磷酸-AKT（P-AKT），磷脂酰肌醇3-激酶（PI3K）和磷酸化PI3K（P-PI3K）的蛋白质表达。通过皮下注射用SH-Neat1和SH-NC稳定地转染ME180细胞来建立动物模型。与正常肿瘤和细胞中的那些相比，NEAT1和E2F7的表达上调，而MIR-889-3P的表达在CC肿瘤和细胞中下调。通过荧光素酶报告系统和RIP测定法证明了MiR-889-3P和Neat1或E2F7之间的相互作用。此外，MIR-889-3P抑制剂抑制了对CC细胞增殖，迁移和侵袭以及CC细胞凋亡的促进作用的Neat1沉默诱导的抑制作用。始终如一地，E2F7逆转了CC中细胞进展的miR-889-3P介导的抑制。此外，通过PI3K / AKT途径靶向MIR-889-3P / E2F7轴来调制细胞行为。最后，甜点1受阻肿瘤生长的干预体内。因此，Neat1通过靶向miR-889-3p来促进CC中的细胞进展，以促进E2F7通过激活PI3K / AKT途径，代表CC的替代靶向治疗。

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    《RSC Advances》 |2019年第59期|共9页
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