Long non-coding RNAs and microRNAs are functional regulators in tumour progression. Herein, we revealed the level LINC02163 was up-regulated in CRC tissues and cell lines, and the expression of LINC02163 negatively correlated with prognosis of CRC patients. Functional experiments demonstrated knockdown of LINC02163 significantly attenuated CRC cells proliferation and metastasis. Mechanism analysis showed miR-511-3p could bind LINC02163 and AKT3, and the expressional level of miR-511-3p negatively correlated with the abundance of LINC02163 and AKT3. Inhibition of LINC02163 suppressed cell proliferation, while transfection of miR-511-3p inhibitor or AKT3 in LINC02163-depletion cells restored cell growth and abolished the cell cycle arrest in G0/G1 phase. Therefore, it was indicated that LINC02163 exerted pro-tumour effect through miR-511-3p/AKT3 axis and was prognostic marker for colorectal cancer.

中文翻译：

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LINC02163通过miR-511-3p / AKT3轴促进结直肠癌的进展。

长的非编码RNA和微小RNA是肿瘤进展中的功能调节因子。在本文中，我们揭示了在CRC组织和细胞系中LINC02163的水平上调，并且LINC02163的表达与CRC患者的预后呈负相关。功能实验表明，敲低LINC02163可以显着减弱CRC细胞的增殖和转移。机理分析表明，miR-511-3p可以结合LINC02163和AKT3，miR-511-3p的表达水平与LINC02163和AKT3的丰度负相关。抑制LINC02163可抑制细胞增殖，而在LINC02163耗尽的细胞中转染miR-511-3p抑制剂或AKT3可恢复细胞生长并消除G0 / G1期的细胞周期停滞。因此，