Long noncoding RNAs (lncRNAs) have been reported to be involved in cancer initiation and evolution, including colorectal cancer (CRC). Nuclear-enriched abundant transcript 1 (NEAT1) exerts important functions in multiple cancers; however, the specific modulatory mechanism in CRC demands in-depth exploration. The expression levels of NEAT1, microRNA-195-5p (miR-195-5p), and centrosomal protein 55 (CEP55) were examined using quantitative real-time polymerase chain reaction (qRT-PCR), and protein expression of CEP55 was detected by Western blot assay. Cell proliferation and apoptosis were measured by 3-(4,5-dimethylthiazole-2-y1)-2,5-diphenyl tetrazolium bromide (MTT) assay and flow cytometry. Transwell migration and invasion assays were applied to evaluate cell metastasis ability. Dual-luciferase reporter assay was used to analyze the correlation among NEAT1, miR-195-5p and CEP55. The expression of NEAT1 was up-regulated in CRC tissues and cells, and overall survival was lower with high expression of NEAT1. Knockdown of NEAT1 repressed cell proliferation, migration, and invasion, while inducing apoptosis in CRC cells. NEAT1 targeted miR-195-5p and inhibited the expression of miR-195-5p. Silence of NEAT1 inhibited CRC cell proliferation, migration, and invasion, and promoted apoptosis by up-regulating miR-195-5p. MiR-195-5p targeted and suppressed CEP55 expression, and CEP55 reverted the effects induced by miR-195-5p. NEAT1 regulated the expression of CEP55 through miR-195-5p. NEAT1 promotes colorectal cancer cellular processes by regulating CEP55 expression via the sponging of miR-195-5p. Therefore, NEAT1 might play a crucial role in CRC treatments.

中文翻译：

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长非编码RNA NEAT1在结直肠癌中的潜力评估。

据报道，长的非编码RNA（lncRNA）与癌症的发生和发展有关，包括结直肠癌（CRC）。富含核的丰富转录本1（NEAT1）在多种癌症中发挥重要作用；但是，CRC中的特定调节机制需要深入研究。使用定量实时聚合酶链反应（qRT-PCR）检测NEAT1，microRNA-195-5p（miR-195-5p）和中心体蛋白55（CEP55）的表达水平，并通过以下方法检测CEP55的蛋白表达蛋白质印迹分析。细胞增殖和凋亡通过3-（4,5-二甲基噻唑-2-y1）-2,5-二苯基溴化四氮唑（MTT）测定和流式细胞仪进行测量。Transwell迁移和侵袭试验用于评估细胞转移能力。采用双荧光素酶报告基因分析法分析NEAT1，miR-195-5p和CEP55之间的相关性。NEAT1的表达在CRC组织和细胞中上调，而高表达的NEAT1则降低了总生存期。抑制NEAT1抑制细胞增殖，迁移和侵袭，同时诱导CRC细胞凋亡。NEAT1靶向miR-195-5p，并抑制miR-195-5p的表达。NEAT1沉默可通过上调miR-195-5p抑制CRC细胞增殖，迁移和侵袭，并促进细胞凋亡。MiR-195-5p靶向并抑制了CEP55的表达，CEP55还原了miR-195-5p诱导的作用。NEAT1通过miR-195-5p调节CEP55的表达。NEAT1通过调节miR-195-5p的海绵状表达来调节CEP55的表达，从而促进结直肠癌的细胞过程。因此，