OBJECTIVE Abundant evidence has illustrated that long non-coding RNA (lncRNA) plays a vital role in the regulation of tumor development and progression. Ectopic expression of a novel lncRNA, termed lnc-AGER-1, has been discovered in cancers, and this lncRNA was reported to exert an anti-tumor effect. However, its biological mechanism remains unelucidated in colorectal cancer. METHODS A total of 159 paired colorectal cancer specimens and adjacent tissues was applied to detect the expression of lnc-AGER-1 by the quantitative Real-time PCR (qRT-PCR), and a series of functional assays was executed to uncover the role of this lncRNA on colorectal cancer. RESULTS We found that the expression of lnc-AGER-1 in the tumor tissues was significantly down-regulated, while compared with adjacent normal tissues (0.0115 ± 0.0718 vs. 0.0347 ± 0.157; P < 0.0001). Also, lnc-AGER-1 was observably associated with clinical T status (r = -0.184, P = 0.024). Patients with advanced T status exerted a significantly lower level of lnc-AGER-1 than those with early T status (20.0% vs. 40.7%, P = 0.021). Over-expression of lnc-AGER-1 inhibited cell proliferation and migration efficiency, and induced cell cycle arrest at the G0/G1 phase, and promoted cell apoptosis. Further research proved that lnc-AGER-1 altered the expression of its neighbor gene, AGER, through acting as a competing endogenous RNA for miR-182 in colorectal cancer. CONCLUSION lnc-AGER-1 has a suppressive role in colorectal cancer development via modulating AGER, which may serve as a target for colorectal cancer diagnosis and treatment.

中文翻译：

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长链非编码 RNA AGER-1 通过海绵化 miR-182 抑制结直肠癌进展。

目的 大量证据表明，长链非编码RNA（lncRNA）在调控肿瘤发展和进展中发挥着至关重要的作用。已经在癌症中发现了一种称为 lnc-AGER-1 的新型 lncRNA 的异位表达，据报道这种 lncRNA 具有抗肿瘤作用。然而，其在结直肠癌中的生物学机制仍未阐明。方法对159对结直肠癌标本及癌旁组织进行定量实时荧光定量PCR（qRT-PCR）检测lnc-AGER-1的表达，并进行一系列功能检测以揭示其作用。这个 lncRNA 对结直肠癌。结果我们发现肿瘤组织中lnc-AGER-1的表达明显下调，而与邻近的正常组织相比（0.0115±0.0718 vs. 0.0347±0.157；P < 0. 0001)。此外，lnc-AGER-1 与临床 T 状态明显相关（r = -0.184，P = 0.024）。晚期 T 状态患者的 lnc-AGER-1 水平显着低于早期 T 状态患者（20.0% vs. 40.7%，P = 0.021）。lnc-AGER-1过表达抑制细胞增殖和迁移效率，诱导细胞周期停滞在G0/G1期，促进细胞凋亡。进一步的研究证明，lnc-AGER-1 通过在结直肠癌中充当 miR-182 的竞争性内源性 RNA，改变了其相邻基因 AGER 的表达。结论 lnc-AGER-1通过调节AGER在结直肠癌发展中具有抑制作用，可作为结直肠癌诊治的靶点。晚期 T 状态患者的 lnc-AGER-1 水平显着低于早期 T 状态患者（20.0% vs. 40.7%，P = 0.021）。lnc-AGER-1过表达抑制细胞增殖和迁移效率，诱导细胞周期停滞在G0/G1期，促进细胞凋亡。进一步的研究证明，lnc-AGER-1 通过在结直肠癌中充当 miR-182 的竞争性内源性 RNA，改变了其相邻基因 AGER 的表达。结论 lnc-AGER-1通过调节AGER在结直肠癌发展中具有抑制作用，可作为结直肠癌诊治的靶点。晚期 T 状态患者的 lnc-AGER-1 水平显着低于早期 T 状态患者（20.0% vs. 40.7%，P = 0.021）。lnc-AGER-1过表达抑制细胞增殖和迁移效率，诱导细胞周期停滞在G0/G1期，促进细胞凋亡。进一步的研究证明，lnc-AGER-1 通过在结直肠癌中充当 miR-182 的竞争性内源性 RNA，改变了其相邻基因 AGER 的表达。结论 lnc-AGER-1通过调节AGER在结直肠癌发展中具有抑制作用，可作为结直肠癌诊治的靶点。lnc-AGER-1过表达抑制细胞增殖和迁移效率，诱导细胞周期停滞在G0/G1期，促进细胞凋亡。进一步的研究证明，lnc-AGER-1 通过在结直肠癌中充当 miR-182 的竞争性内源性 RNA，改变了其相邻基因 AGER 的表达。结论 lnc-AGER-1通过调节AGER在结直肠癌发展中具有抑制作用，可作为结直肠癌诊治的靶点。lnc-AGER-1过表达抑制细胞增殖和迁移效率，诱导细胞周期停滞在G0/G1期，促进细胞凋亡。进一步的研究证明，lnc-AGER-1 通过在结直肠癌中充当 miR-182 的竞争性内源性 RNA，改变了其相邻基因 AGER 的表达。结论 lnc-AGER-1通过调节AGER在结直肠癌发展中具有抑制作用，可作为结直肠癌诊治的靶点。