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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：长非编码RNA NEAT1通过激活PI3K / AKT通路来调节miR-889-3p / E2F7轴，从而加速宫颈癌的细胞进程

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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，通常在女性中被诊断出来。显然，长的非编码RNA核富集常染色体转录本1（NEAT1）已被确定为多种癌症中的肿瘤启动子。我们的研究集中于lncRNA NEAT1对子宫颈癌细胞进程的影响以及NEAT1对CC细胞进程的潜在分子机制。通过定量实时聚合酶链反应（qRT-PCR）测量CC肿瘤和细胞中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）分析进行了验证。细胞计数试剂盒8（CCK-8）和流式细胞仪用于细胞增殖和凋亡评估。通过transwell测定法检查细胞迁移和侵袭。 E2F7，AKT，磷酸-AKT（p-AKT），磷脂酰肌醇3-激酶（PI3K）和磷酸化的PI3K（p-PI3K）的蛋白质表达通过蛋白质印迹分析进行了分析。通过皮下注射稳定转染了sh-NEAT1和sh-NC的Me180细胞，建立了动物模型。与正常肿瘤和细胞相比，CC肿瘤和细胞中NEAT1和E2F7的表达上调，而miR-889-3p的表达则下调。通过荧光素酶报告系统和RIP分析证明了miR-889-3p与NEAT1或E2F7之间的相互作用。另外，miR-889-3p抑制剂减弱了NEAT1沉默诱导的对细胞增殖，迁移和侵袭的抑制作用，以及对CC细胞凋亡的促进作用。一致地，E2F7逆转了miR-889-3p介导的CC细胞抑制作用。此外，NEAT1通过PI3K / AKT途径靶向miR-889-3p / E2F7轴来调节细胞行为。最后，NEAT1的干预阻碍了体内肿瘤的生长。因此，NEAT1通过靶向miR-889-3p通过激活PI3K / AKT途径促进E2F7表达，从而促进CC细胞的发展，代表了CC的替代靶向治疗。

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