We planned to investigate the possible influences of long non-coding RNA (opioid growth factor receptor pseudogene 1) OGFRP1 in endometrial cancer and its potential regulatory mechanism. We measured the level of OGFRP1 in endometrial cancer tissues and evaluated the influences of OGFRP1 dysregulation on the tumour cell biological processes of endometrial cancer cells. Further, the regulatory relationships between OGFRP1 and miR-124-3p, between miR-124-3p and Sirtuin1 (SIRT1) were, respectively, investigated. The interaction between OGFRP1 dysregulation and activation of PI3K/AKT/GSK-3β pathway was revealed by Western blotting. OGFRP1 was up-regulated in endometrial cancer tissues and cells. OGFRP1 suppression inhibited the malignant behaviour (inhibited cell viability, promoted cell apoptosis, and suppressed cell migration and invasion) of the Ishikawa cells via negatively regulating miR-124-3p. SIRT1 was a target gene of miR-124-3p, and miR-124-3p regulated tumour growth and metastasis by the down-stream signal of SIRT1. Moreover, suppression of OGFRP1 restrained the activation of PI3K/AKT/GSK-3β signals in the Ishikawa cells via miR-124-3p/SIRT1 axis. Our experiments revealed that upregulation of OGFRP1 may enhance the progression of endometrial cancer by regulating miR-124-3p/SIRT1 axis and by activating PI3K/AKT/GSK-3β pathway. OGFRP1 may be of significance in illustrating the biology of endometrial cancer.

中文翻译：

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较长的非编码RNA OGFRP1的上调通过调节miR-124-3p / SIRT1轴并激活PI3K / AKT /GSK-3β途径来促进子宫内膜癌。

我们计划调查长非编码RNA（阿片类生长因子受体假基因1）OGFRP1在子宫内膜癌中的可能影响及其潜在的调控机制。我们测量了子宫内膜癌组织中OGFRP1的水平，并评估了OGFRP1失调对子宫内膜癌细胞的肿瘤细胞生物学过程的影响。此外，分别研究了OGFRP1与miR-124-3p之间，miR-124-3p与Sirtuin1（SIRT1）之间的调节关系。通过蛋白质印迹揭示了OGFRP1失调与PI3K / AKT /GSK-3β途径活化之间的相互作用。OGFRP1在子宫内膜癌组织和细胞中上调。OGFRP1抑制可抑制恶性行为（抑制细胞生存力，促进细胞凋亡，并通过负调控miR-124-3p抑制了石川细胞的迁移和侵袭。SIRT1是miR-124-3p的靶基因，miR-124-3p通过SIRT1的下游信号调节肿瘤的生长和转移。此外，OGFRP1的抑制通过miR-124-3p / SIRT1轴抑制了Ishikawa细胞中PI3K / AKT /GSK-3β信号的激活。我们的实验表明，通过调节miR-124-3p / SIRT1轴并激活PI3K / AKT /GSK-3β途径，OGFRP1的上调可能会促进子宫内膜癌的进展。OGFRP1在说明子宫内膜癌的生物学过程中可能具有重要意义。OGFRP1的抑制通过miR-124-3p / SIRT1轴抑制了Ishikawa细胞中PI3K / AKT /GSK-3β信号的激活。我们的实验表明，通过调节miR-124-3p / SIRT1轴并激活PI3K / AKT /GSK-3β途径，OGFRP1的上调可能会促进子宫内膜癌的进展。OGFRP1在说明子宫内膜癌的生物学过程中可能具有重要意义。OGFRP1的抑制通过miR-124-3p / SIRT1轴抑制了Ishikawa细胞中PI3K / AKT /GSK-3β信号的激活。我们的实验表明，通过调节miR-124-3p / SIRT1轴并激活PI3K / AKT /GSK-3β途径，OGFRP1的上调可能会促进子宫内膜癌的进展。OGFRP1在说明子宫内膜癌的生物学过程中可能具有重要意义。