Increasing studies have well-documented the involvement of numerous lncRNAs in regulating the malignant phenotypes of various tumors including non-small cell lung cancer (NSCLC) cells. However, up to date, the effects and mechanism of lncRNA amine oxidase, copper containing 4, pseudogene (AOC4P) in NSCLC progression remain undefined. AOC4P expression in NSCLC cells was detected by qRT-PCR. The protein levels of Wnt/β-catenin pathway-related proteins, matrix metallopeptidase (MMP)-2, and MMP-9 were examined by Western blot. The effects of AOC4P or combined with Wnt agonist BML-284 on the malignant phenotypes in NSCLC cells were explored by CCK-8, Transwell invasion assay, flow cytometry analysis and caspase-3/7 activity. AOC4P was lowly expressed in NSCLC samples and cells. Overexpression of AOC4P inhibited viability, the expression of MMP-2 and MMP-9, and invasion of NSCLC cells. Apoptosis and caspase-3/7 activity were suppressed in response to AOC4P overexpression in NSCLC cells. AOC4P overexpression suppressed tumor growth in a xenograft mouse model. Activation of the Wnt/β-catenin pathway by BML-284 abolished the effects of AOC4P overexpression on cell viability, invasion and apoptosis in NSCLC cells. In conclusion, AOC4P overexpression suppresses viability and invasion and induces apoptosis in NSCLC cells via inhibition of the Wnt/β-catenin pathway.

中文翻译：

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AOC4P通过抑制Wnt /β-catenin途径抑制NSCLC细胞的活力和侵袭并诱导其凋亡。

越来越多的研究充分证明了许多lncRNA参与调节包括非小细胞肺癌（NSCLC）细胞在内的各种肿瘤的恶性表型。然而，迄今为止，lncRNA胺氧化酶，含4铜的假基因（AOC4P）在NSCLC进展中的作用和机制尚不清楚。通过qRT-PCR检测NSCLC细胞中AOC4P表达。用Western blot检测Wnt /β-catenin途径相关蛋白，基质金属肽酶（MMP）-2和MMP-9的蛋白水平。通过CCK-8，Transwell侵袭试验，流式细胞仪分析和caspase-3 / 7活性探讨了AOC4P或与Wnt激动剂BML-284联合对NSCLC细胞恶性表型的影响。AOC4P在NSCLC样品和细胞中低表达。AOC4P的过表达抑制了活力，MMP-2和MMP-9的表达以及对NSCLC细胞的侵袭。响应于ACL4P在NSCLC细胞中的过度表达，凋亡和caspase-3 / 7活性受到抑制。AOC4P过表达抑制异种移植小鼠模型中的肿瘤生长。BML-284对Wnt /β-catenin途径的激活消除了AOC4P过表达对NSCLC细胞活力，侵袭和凋亡的影响。总之，AOC4P过表达通过抑制Wnt /β-catenin途径抑制NSCLC细胞的活力和侵袭并诱导凋亡。BML-284对Wnt /β-catenin途径的激活消除了AOC4P过表达对NSCLC细胞活力，侵袭和凋亡的影响。总之，AOC4P过表达通过抑制Wnt /β-catenin途径抑制NSCLC细胞的活力和侵袭并诱导凋亡。BML-284对Wnt /β-catenin途径的激活消除了AOC4P过表达对NSCLC细胞活力，侵袭和凋亡的影响。总之，AOC4P过表达通过抑制Wnt /β-catenin途径抑制NSCLC细胞的活力和侵袭并诱导凋亡。