Colorectal cancer (CRC) is the third most common cancer diagnosed worldwide. Recently, nucleolar complex protein 14 (NOP14) has been discovered to play a critical role in cancer development and progression, but the mechanisms of action of NOP14 in colorectal cancer remain to be elucidated. In this study, we used collected colorectal cancer tissues and cultured colorectal cancer cell lines (SW480, HT29, HCT116, DLD1, Lovo), and measured the mRNA and protein expression levels of NOP14 in colorectal cancer cells using qPCR and western blotting. GFP-NOP14 was constructed and siRNA fragments against NOP14 were synthesized to investigate the importance of NOP14 for the development of colorectal cells. Transwell migration assays were used to measure cell invasion and migration, CCK-8 kits were used to measure cell activity, and flow cytometry was applied to the observation of apoptosis. We found that both the mRNA and protein levels of NOP14 were significantly upregulated in CRC tissues and cell lines. Overexpression of GFP-NOP14 markedly promoted the growth, migration, and invasion of the CRC cells HT19 and SW480, while genetic knockdown of NOP14 inhibited these behaviors. Overexpression of NOP14 promoted the expression of NRIP1 and phosphorylated inactivation of GSK-3β, leading to the upregulation of β-catenin. Genetic knockdown of NOP14 had the opposite effect on NRIP1/GSK-3/β-catenin signals. NOP14 therefore appears to be overexpressed in clinical samples and cell lines of colorectal cancer, and promotes the proliferation, growth, and metastasis of colorectal cancer cells by modulating the NRIP1/GSK-3β/β-catenin signaling pathway.

结直肠癌 (CRC) 是全球第三大最常见的癌症。最近，已发现核仁复合蛋白 14 (NOP14) 在癌症发生和进展中起关键作用，但 NOP14 在结直肠癌中的作用机制仍有待阐明。在本研究中，我们使用收集的结直肠癌组织和培养的结直肠癌细胞系（SW480、HT29、HCT116、DLD1、Lovo），并使用 qPCR 和蛋白质印迹法测量结直肠癌细胞中 NOP14 的 mRNA 和蛋白质表达水平。构建了 GFP-NOP14 并合成了针对 NOP14 的 siRNA 片段，以研究 NOP14 对结肠直肠细胞发育的重要性。Transwell 迁移测定用于测量细胞侵袭和迁移，CCK-8 试剂盒用于测量细胞活性，并应用流式细胞术观察细胞凋亡。我们发现 NOP14 的 mRNA 和蛋白质水平在 CRC 组织和细胞系中均显着上调。GFP-NOP14 的过表达显着促进了 CRC 细胞 HT19 和 SW480 的生长、迁移和侵袭，而 NOP14 的基因敲低抑制了这些行为。NOP14的过表达促进了NRIP1的表达和GSK-3β的磷酸化失活，导致β-catenin的上调。NOP14 的基因敲低对 NRIP1/GSK-3/β-catenin 信号有相反的影响。因此，NOP14 似乎在结直肠癌的临床样本和细胞系中过度表达，并通过调节 NRIP1/GSK-3β/β-catenin 信号通路促进结直肠癌细胞的增殖、生长和转移。我们发现 NOP14 的 mRNA 和蛋白质水平在 CRC 组织和细胞系中均显着上调。GFP-NOP14 的过表达显着促进了 CRC 细胞 HT19 和 SW480 的生长、迁移和侵袭，而 NOP14 的基因敲低抑制了这些行为。NOP14的过表达促进了NRIP1的表达和GSK-3β的磷酸化失活，导致β-catenin的上调。NOP14 的基因敲低对 NRIP1/GSK-3/β-catenin 信号有相反的影响。因此，NOP14 似乎在结直肠癌的临床样本和细胞系中过度表达，并通过调节 NRIP1/GSK-3β/β-catenin 信号通路促进结直肠癌细胞的增殖、生长和转移。我们发现 NOP14 的 mRNA 和蛋白质水平在 CRC 组织和细胞系中均显着上调。GFP-NOP14 的过表达显着促进了 CRC 细胞 HT19 和 SW480 的生长、迁移和侵袭，而 NOP14 的基因敲低抑制了这些行为。NOP14的过表达促进了NRIP1的表达和GSK-3β的磷酸化失活，导致β-catenin的上调。NOP14 的基因敲低对 NRIP1/GSK-3/β-catenin 信号有相反的影响。因此，NOP14 似乎在结直肠癌的临床样本和细胞系中过度表达，并通过调节 NRIP1/GSK-3β/β-catenin 信号通路促进结直肠癌细胞的增殖、生长和转移。